Create detailed mbbs notes on miscarriage

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"miscarriage"[MeSH Terms]

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types of abortion threatened inevitable incomplete missed ultrasound

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spontaneous abortion ultrasound empty gestational sac missed miscarriage

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Miscarriage (Spontaneous Abortion): MBBS Notes

1. Definitions

  • Miscarriage / spontaneous abortion: spontaneous loss of pregnancy before 20 weeks of gestation. - Swanson's Family Medicine Review. Rosen's gives the same limit. Loss after 20 weeks, or of a fetus over 500 g, is classed as preterm birth/stillbirth. - Rosen's Emergency Medicine, p. 3347.
  • WHO definition: expulsion of a fetus weighing less than 500 g, which corresponds to about 20-22 weeks.
  • Early pregnancy loss: a nonviable intrauterine pregnancy within the first 12 weeks 6 days. It shows either an empty gestational sac, or a sac with an embryo but no cardiac activity. - Rosen's.
  • Recurrent pregnancy loss (RPL): 3 or more consecutive losses in the classical definition. - Swanson's. Newer ASRM/ESHRE guidance uses 2 or more, and evaluation is reasonable after 2 losses. - Berek & Novak's Gynecology, p. 1791.
  • Induced abortion is a different entity. It is deliberate termination, covered in India by the MTP Act.

2. Epidemiology

  • About 15-30% of recognised pregnancies end in miscarriage. RPL (3 or more losses) affects about 1% of women. - Berek & Novak's, p. 1791.
  • About 80% of miscarriages occur in the first trimester. - Rosen's.
  • Up to one-third of detectable pregnancies are lost after implantation. Many losses are never recognised.
  • Bleeding in early pregnancy occurs in about 25% of pregnancies. Up to 50% of those women miscarry before 20 weeks.
  • If fetal cardiac activity is seen on ultrasound, the miscarriage risk falls to about 3-6%.

3. Risk factors

CategoryFactors
Maternal ageRisk rises sharply after 35. It is about 5 times higher at over 40 than at 25-29 years.
PaternalAdvanced paternal age
Past historyPrevious miscarriage
LifestyleSmoking, alcohol, cocaine, heavy caffeine, obesity, very low BMI, stress
MedicalPoorly controlled diabetes, thyroid disease, SLE/antiphospholipid syndrome, PCOS, thrombophilias
UterineCongenital anomalies, fibroids, intrauterine adhesions, cervical insufficiency
InfectionMaternal infections
OtherIncreased parity, history of bleeding this pregnancy
Source for the list above: Rosen's, p. 3347.
Diabetes: type 2 diabetes raised the miscarriage rate to 25%, against 19.7% in women without diabetes (RR 1.28). Type 1 diabetes showed no significant rise (RR 0.91). - Creasy & Resnik's Maternal-Fetal Medicine, p. 1435. Periconceptional glycaemic control is what matters.

4. Aetiology

A. Fetal / genetic (most common cause of first-trimester loss)

  • Fetal aneuploidy is the commonest cause of first-trimester miscarriage. - Berek & Novak's, p. 1791.
  • Autosomal trisomies account for about half of chromosomal losses. Trisomy 16 is the commonest.
  • Monosomy X (45,X) is the next commonest, followed by triploidy and tetraploidy.
  • Most chromosomal errors arise sporadically. Examples are maternal meiotic nondisjunction, which increases with age, and dispermy.
  • Structural errors, such as balanced translocation in a parent, are more important in RPL.
  • Anembryonic gestation (blighted ovum): the ovum never develops.

B. Maternal causes

1. Anatomical (more typical of second-trimester loss)
  • Cervical insufficiency: painless dilatation, usually at 16-24 weeks.
  • Uterine septum (the most strongly associated congenital anomaly), bicornuate uterus.
  • Submucous fibroids, Asherman syndrome (intrauterine adhesions).
2. Endocrine
  • Luteal phase defect (controversial), uncontrolled diabetes.
  • Thyroid disease (hypothyroidism, thyroid autoimmunity).
  • PCOS, hyperprolactinaemia.
3. Immunological
  • Antiphospholipid syndrome (APS): the most important treatable cause of RPL.
  • SLE.
  • Alloimmune factors, which remain controversial.
4. Thrombophilias
  • Inherited: factor V Leiden, prothrombin mutation, protein C/S and antithrombin deficiency.
  • The link is stronger for second-trimester and later losses.
5. Infections (rarely the true cause of RPL)
  • Listeria, Toxoplasma, rubella, CMV, HSV, syphilis, malaria, bacterial vaginosis.
6. Environmental / drugs
  • Alcohol, tobacco, cocaine, radiation, and anaesthetic gases.
  • Teratogens such as methotrexate and misoprostol.
7. Trauma and surgery
  • Abdominal surgery and trauma.

C. Paternal / male factors

  • Sperm DNA fragmentation and structural chromosomal abnormalities.

D. Mechanism

Fetal death precedes clinical miscarriage, often by several weeks. Ultrasound shows death before 8 weeks in most cases, although symptoms are commonest at 8-12 weeks. Decidual haemorrhage and necrosis follow. The conceptus separates, becomes a foreign body, and the uterus contracts to expel it. - Rosen's.

5. Classification and clinical types

TypeCervical osFindings
ThreatenedClosedVaginal bleeding (often light), with or without mild cramps. The pregnancy remains viable.
InevitableOpen (dilated)Bleeding and cramping. No tissue has passed yet. Expulsion cannot be prevented.
IncompleteOpenPartial expulsion. Products of conception are in the canal or vagina. Heavy bleeding with colicky pain.
CompleteClosedEverything has been expelled. Bleeding and pain settle. The uterus is contracted and empty on ultrasound.
Missed (delayed / silent)ClosedEmbryo or fetus dead but retained. Pregnancy symptoms regress, there is a brownish discharge, and the uterus is smaller than dates.
SepticOpenMiscarriage complicated by intrauterine infection.
Recurrent (habitual)-3 or more consecutive losses.
Sources: Swanson's; Rosen's, pp. 3347-3348.
Points to remember
  • Threatened miscarriage carries a 35-50% risk of progressing, depending on risk factors and severity. - Rosen's.
  • "Missed abortion" is considered an obsolete term. Preferred terms are anembryonic gestation, early fetal demise and delayed miscarriage. - Rosen's.
  • History does not reliably classify the type of miscarriage, and symptom severity does not predict outcome. The pelvic examination and ultrasound do. - Rosen's.
  • To diagnose a complete miscarriage you need one of these:
    • a gestational sac seen being passed;
    • histology showing products of conception;
    • an empty uterus on ultrasound after a known intrauterine pregnancy;
    • a return to a negative pregnancy test.

Ultrasound-based terms

  • Embryonic or fetal demise: embryonic pole or crown-rump length of 5-40 mm without cardiac activity. - Swanson's.
  • Anembryonic pregnancy: a gestational sac without an embryo.

6. Clinical features

History

  • Gestational age and LMP.
  • Pregnancy symptoms, and whether they have disappeared. Loss of nausea and breast tenderness suggests a missed miscarriage.
  • Amount and duration of bleeding, clots, passage of tissue.
  • Cramping, lower abdominal or back pain.
  • Fever, foul discharge (sepsis), and any attempt to induce abortion.
  • Previous losses, medical illness, medications and exposures.

Examination

  1. General: pulse, BP, pallor, temperature. Shock is out of proportion to visible blood loss in cervical shock.
  2. Abdomen:
    • tenderness or peritonism, which suggests ectopic pregnancy or sepsis;
    • the uterus should not normally be palpable abdominally in the first trimester.
  3. Speculum:
    • find the bleeding source;
    • check whether the os is open or closed;
    • look for tissue at the os.
  4. Bimanual: uterine size against dates, cervical motion tenderness, adnexal mass.
Cervical probing should NOT be done in second- and third-trimester bleeding. A placenta praevia may be present. - Rosen's.

7. Differential diagnosis of early pregnancy bleeding

  • Ectopic pregnancy is the most important one to exclude. Adnexal tenderness should always raise this possibility. - Rosen's.
  • Hydatidiform mole (vesicular "snowstorm" appearance on ultrasound, very high hCG).
  • Implantation bleeding.
  • Cervical or vaginal causes: polyp, ectropion, cervicitis, trauma, carcinoma.
  • Subchorionic haematoma.
  • PID, which is less common in pregnancy.

8. Investigations

  1. Haemoglobin and blood group with Rh type. This is mandatory. - Rosen's.
  2. Urine pregnancy test (qualitative) and serum β-hCG (quantitative).
  3. Transvaginal ultrasound is the primary diagnostic tool. - Rosen's.
  4. Serial hCG every 48-72 hours when the location of the pregnancy is uncertain. In a normal early intrauterine pregnancy, hCG rises by about 53-66% in 48 hours. A slow rise or a fall suggests an abnormal pregnancy.
  5. Other: CBC, CRP, and blood and high vaginal swab cultures if septic. Coagulation profile in a severely ill patient.

Ultrasound landmarks (transvaginal)

FindingWeeks from LMPβ-hCG (mIU/mL)
Gestational sac5about 1000
Discriminatory zone5-61000-2000
Yolk sac6about 2000
Fetal pole7about 5700
Cardiac activity6-7about 7000
Source: Rosen's, Table 173.1. These values vary between machines and units, so use them as a guide only.

Diagnostic criteria for pregnancy failure

  • The 2013 Society of Radiologists in Ultrasound consensus is stricter than the older criteria in Rosen's Box 173.1. This is from my own knowledge, not from the library texts.
  • Definitive criteria for failure:
    • CRL of 7 mm or more with no heartbeat;
    • mean sac diameter of 25 mm or more with no embryo;
    • no embryo with heartbeat 2 or more weeks after a scan showing a gestational sac without a yolk sac.
  • Suspicious but not diagnostic:
    • CRL under 7 mm with no heartbeat;
    • mean sac diameter of 16-24 mm with no embryo;
    • empty amnion.
  • In doubtful cases, repeat the scan in 7-10 days. Do not intervene on borderline findings, because a viable pregnancy can be harmed.

9. Management

First ask about the woman's pregnancy intentions. About 50% of pregnancies are unintended, and her goals may change management. - Berek & Novak's, p. 1752.

A. General steps

  1. Assess haemodynamic status. Resuscitate with IV access, fluids and blood if she is unstable.
  2. Send blood group and Rh type, and cross-match if bleeding is heavy.
  3. Give anti-D immunoglobulin to Rh-negative women. Rosen's recommends it for all pregnant patients with bleeding in the ED:
    • 50 μg (some use 120 μg) in the first trimester;
    • 300 μg after the first trimester.
  4. Exclude ectopic pregnancy.
  5. Give psychological support. Reassure her that she did nothing to cause it. Grief is normal. - Rosen's, p. 3349.

B. By type

1. Threatened miscarriage
  • No treatment is proven to prevent miscarriage. - Rosen's.
  • Reassurance and counselling.
  • Rest and bed rest do not change the outcome. Moderate daily activity is safe.
  • Avoid intercourse and tampons while bleeding.
  • Paracetamol for pain.
  • Review with ultrasound and repeat hCG if the location is uncertain.
  • Return precautions: heavy bleeding, fever, severe pain, fainting.
  • Some guidelines suggest progesterone for women with early bleeding and a history of previous miscarriage (see section 11).
2. Inevitable / incomplete miscarriage
  • Brisk bleeding: remove tissue from the cervical os with ring forceps. This often slows the bleeding, and a vasovagal bradycardia also responds to removing the tissue. - Berek & Novak's, p. 1751.
  • Give oxytocin or ergometrine if bleeding is heavy (ergometrine is contraindicated in hypertension).
  • Evacuate the uterus (suction evacuation, or manual vacuum aspiration up to 12 weeks).
  • If febrile, treat as septic and give broad-spectrum antibiotics.
3. Missed miscarriage / anembryonic pregnancy Three options. - Berek & Novak's, p. 1752.
OptionDetails
ExpectantSuccess: incomplete 91%, missed 76%, anembryonic 66%. It may take 4-8 weeks. It carries more unplanned surgery, bleeding and transfusion, with no difference in infection.
MedicalMisoprostol 800 μg vaginally (ACOG), with up to 84% success for missed abortion. 600 μg sublingually is also acceptable. For incomplete abortion, 600 μg orally or 400 μg sublingually gives over 90% success. Pretreatment with mifepristone 200 mg 24 hours earlier improved success (83% against 67% with misoprostol alone).
SurgicalSuction curettage / manual vacuum aspiration. Indicated for heavy bleeding, unstable vitals, a patient's preference, or unreliable follow-up.
Surgical evacuation is also preferred when there is retained tissue with infection and when coagulopathy is a concern.
4. Complete miscarriage
  • Confirm with ultrasound, and no evacuation is needed.
  • Counsel, follow up, and check the hCG falls to negative.
5. Septic miscarriage
  • Triad: fever, bleeding and lower abdominal pain, often with foul discharge.
  • The organisms are usually polymicrobial: E. coli, Bacteroides, anaerobic streptococci, Clostridium perfringens.
  • Management:
    • IV broad-spectrum antibiotics (for example ampicillin or a cephalosporin, plus gentamicin and metronidazole);
    • evacuate the uterus after starting antibiotics, usually within hours;
    • fluids, oxygen, and ICU care for shock;
    • tetanus prophylaxis, and exclude uterine or bowel injury if instrumentation was attempted;
    • hysterectomy if there is gas gangrene or failure to respond.

C. Cervical insufficiency

  • Painless cervical dilatation in the second trimester, followed by bulging membranes and a painless delivery of a live-appearing or recently dead fetus.
  • Diagnosis is by history and ultrasound cervical length (under 25 mm before 24 weeks).
  • Treatment: cervical cerclage (McDonald or Shirodkar), done at 12-14 weeks, with removal at 36-37 weeks. It can be placed as an emergency (rescue) procedure if the membranes are not yet infected. Vaginal progesterone is an alternative for a short cervix without prior preterm birth.

10. Complications of miscarriage

ComplicationNotes
HaemorrhageCan cause shock.
SepsisSeptic shock, DIC, acute renal failure, pelvic abscess, peritonitis.
Retained productsPersistent bleeding.
Asherman syndromeAfter vigorous curettage. Leads to amenorrhoea and infertility.
Cervical or uterine injuryPerforation during evacuation.
Rh isoimmunisationIf anti-D is not given.
PsychologicalGrief, depression, anxiety.
Gestational trophoblastic diseaseMissed in rare cases. Send tissue for histology if suspicious.

11. Recurrent pregnancy loss (RPL)

Definition and frequency

  • Three or more consecutive losses (1% of women). Evaluate after 2 losses. - Berek & Novak's, p. 1791.
  • The evaluation yield is similar for couples with 2 or 3 losses. - Berek & Novak's.

Causes, in order

Genetic, thrombophilias, anatomical, endocrine, infection, immunological (cellular and humoral/APS), male factors, environmental. - Berek & Novak's, chapter outline. In practice about half of couples have no identifiable cause (unexplained RPL).

Evaluation (couple)

  1. History and examination: timing of previous losses, the family history, medical illness, medications.
  2. Antiphospholipid antibodies: lupus anticoagulant, anticardiolipin IgG/IgM, anti-β2-glycoprotein I. Repeat positive tests at 12 weeks or later.
  3. Parental karyotype: to look for balanced translocation.
  4. Uterine cavity: 3D ultrasound, sonohysterography, hysterosalpingography, hysteroscopy or MRI.
  5. Endocrine: TSH, HbA1c or glucose, prolactin if there are menstrual abnormalities.
  6. Products of conception karyotype from the next loss is useful.
  7. Thrombophilia screen: only in selected cases (for example second-trimester loss or a family history).
Tests of unproven value include routine testing for NK cells, HLA typing, and TORCH screens.

Treatment

CauseTreatment
Antiphospholipid syndromeLow-dose aspirin plus LMWH (heparin) from a positive pregnancy test.
Parental translocationGenetic counselling, prenatal diagnosis, PGT as an option.
Uterine septumHysteroscopic septum resection (benefit still debated).
Cervical insufficiencyCerclage.
Hypothyroidism / diabetesOptimise before conception.
UnexplainedSupportive care ("TLC") gives a good chance of a live birth. Progesterone helped in women with early bleeding and a history of losses. Immunotherapy (leukocyte immunisation, IVIG) is not recommended.
Treatment categories from Berek & Novak's, Chapter 33 outline; specific regimens are from my own knowledge.
Prognosis: even after 3 losses with no identified cause, the chance of a live birth in the next pregnancy is about 60-75%.

12. Prevention and counselling

  • Preconception folic acid, optimal control of diabetes and thyroid disease.
  • Stop smoking, alcohol and drugs, and limit caffeine.
  • Maintain a healthy BMI.
  • Early booking and early scan in women with a history of losses.
  • Counselling for the next pregnancy: usually safe to try after one normal period or when emotionally ready. Contraception is needed in the meantime.

13. Medicolegal and Indian context (from my own knowledge)

  • Induced abortion in India is regulated by the MTP Act 1971, amended in 2021. Abortion is permitted up to 20 weeks on the opinion of one registered medical practitioner, and 20-24 weeks on the opinion of two for specified categories of women. Beyond 24 weeks it requires a medical board, for substantial fetal abnormalities.
  • Unsafe induced abortion remains a notable cause of maternal mortality. - Berek & Novak's, p. 776 (global figure of 47,000 deaths a year).
  • Criminal abortion and septic abortion are common forensic topics.

14. High-yield MCQ and viva points

  1. Commonest cause of first-trimester miscarriage: chromosomal abnormality, especially trisomy 16.
  2. Commonest cause of second-trimester miscarriage: cervical insufficiency and uterine anomalies.
  3. Threatened miscarriage: closed os. Inevitable: open os.
  4. Missed miscarriage: the uterus is smaller than dates, there is a brown discharge, and the pregnancy test turns negative later.
  5. Test of choice to confirm viability and location: transvaginal ultrasound.
  6. Treatable cause of RPL with proven treatment: antiphospholipid syndrome, treated with aspirin plus heparin.
  7. Medical management: mifepristone 200 mg then misoprostol 800 μg.
  8. Always check blood group and Rh, and give anti-D if Rh-negative.
  9. Cervical cerclage: McDonald (simple purse-string) and Shirodkar (dissection of bladder, suture placed at the internal os).
  10. Painless dilatation and delivery in the second trimester means cervical insufficiency.
  11. Never probe the cervix in late second or third-trimester bleeding.
  12. First step in a septic miscarriage: antibiotics, then evacuation.

Recent literature check

I searched PubMed for systematic reviews and meta-analyses from the last two years. The three results were qualitative reviews of women's coping strategies and healthcare experiences after miscarriage (PMIDs 41317448, 41561995, 37559182). They do not contradict the clinical management above. They do support its emphasis on empathic communication, follow-up and psychological support.
Sources: Berek & Novak's Gynecology (pp. 776, 1751-1753, 1791); Rosen's Emergency Medicine (pp. 3347-3349); Creasy & Resnik's Maternal-Fetal Medicine (p. 1435); Swanson's Family Medicine Review. Items marked "from my own knowledge" (SRU criteria, MTP Act, exact RPL regimens, septic abortion antibiotics) were not checked against the library and should be confirmed in your prescribed textbook, such as Dutta's Obstetrics.
I can turn this into a one-page revision sheet or a set of practice MCQs if that would help.

Maternal changes during pregnancy. Make sure to also include point given form shaws textbook of gynaecology and mudaliar textbook of clinical obg

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"pregnancy"[MeSH Terms] AND "adaptation, physiological"[MeSH Terms]

Maternal Changes During Pregnancy: MBBS Notes

A note on your two textbooks. Shaw's Textbook of Gynaecology and Mudaliar's Clinical Obstetrics are not in my library. I can't see their pages, so I can't quote them or tell you which points they stress.
  • Library-sourced points are cited to the books I could open: Creasy & Resnik's, Barash's Clinical Anesthesia, Miller's Anesthesia, Tintinalli's, Brenner & Rector's The Kidney, Dikshit's Forensic Medicine and Berek & Novak's.
  • Points marked (std) come from my own knowledge of the standard Indian-textbook content. They are not checked against Shaw's or Mudaliar's.
  • Shaw's is a gynaecology text, so the main source for this topic in your set is probably Mudaliar. If you paste or photograph the relevant pages, I'll merge them into these notes.

1. Overview

Maternal adaptation serves three purposes:
  1. To support fetal growth and the placenta.
  2. To prepare the mother for labour and blood loss.
  3. To prepare for lactation.
The drivers are the placental hormones (hCG, oestrogen, progesterone, hPL, relaxin), mechanical pressure from the growing uterus, and the increased metabolic demand.

2. Genital tract

Uterus

  • Weight: about 70 g non-pregnant to about 1000-1100 g at term. Capacity: 10 mL to about 5 L. (std)
  • Mechanism: early on, hypertrophy of existing muscle fibres under oestrogen and progesterone, plus some hyperplasia. Later growth is stretching. (std)
  • Growth in height (Tintinalli's):
    • At 12 weeks the fundus reaches the pubic symphysis and the uterus becomes an abdominal organ.
    • At 20 weeks it reaches the umbilicus.
    • After that it grows about 1 cm per week above the umbilicus.
    • At 36 weeks it reaches the xiphisternum (std). Fundal height falls slightly at 38-40 weeks with engagement.
  • Shape: pyriform, then globular at about 12 weeks, then ovoid. (std)
  • Dextrorotation: the uterus rotates to the right because of the rectosigmoid on the left. (std)
  • Isthmus: hypertrophies and softens, and is taken up into the lower uterine segment after 12 weeks. Hegar's sign is positive at about the 6th week (isthmus softness). (Forensic Medicine texts)
  • Uterine contractions: painless, irregular Braxton Hicks contractions appear from early pregnancy and are felt more in the 2nd-3rd trimesters. (Guyton)
  • Uterine blood flow: rises to about 500-700 mL/min at term, roughly 10-12% of cardiac output. (std) Uterine flow increases markedly, so uterine injury can cause severe haemorrhage. (Tintinalli's)
  • Placental bed: the spiral arteries undergo trophoblastic remodelling, which gives a low-resistance flow.

Cervix

  • Goodell's sign: softening, from increased vascularity and oedema. (Forensic texts)
  • Bluish colour (Chadwick's sign, see vagina) and hypertrophy and hyperplasia of the cervical glands.
  • Mucus plug (operculum): thick mucus fills the canal and protects against ascending infection. (std)
  • Eversion of the endocervical columnar epithelium (ectropion) may occur, and the cervix bleeds easily on contact.

Vagina and vulva

  • Chadwick's / Jacquemier's sign: the vaginal mucosa changes from pink to violet and then blue because of increased vascularity and venous obstruction. It is seen from about the 4th week. - Dikshit, Forensic Medicine; Parikh's; Berek & Novak's
  • Increased secretions that are thick and white, with a lower, more acidic pH (std). Glycogen deposition favours Lactobacillus and moniliasis (candidiasis).
  • Softening and hypertrophy of the vaginal wall, and vulval varicosities. Osiander's sign (pulsation in the lateral fornix) is also described.

Ovaries and tubes

  • Ovulation stops and follicular maturation is suppressed.
  • The corpus luteum of pregnancy is maintained by hCG and secretes progesterone up to about 8-10 weeks. After that the placenta takes over (the luteo-placental shift). (std)
  • The tubes lengthen and are displaced upward. Decidual reaction may appear on the ovarian surface.

Breasts

  • Enlargement, tingling and heaviness from the 6th week.
  • Increased vascularity with visible superficial veins.
  • Nipple and areola darken (primary areola), then a secondary areola develops by about 20 weeks. Montgomery's tubercles enlarge.
  • Colostrum can be expressed from about 12-16 weeks. Lactation is held back until delivery by high oestrogen and progesterone, then released when they fall and prolactin acts. (std)

3. Cardiovascular system

Key changes (summary table)

ParameterChangeDetails
Total blood volumeUp about 40-50%Rises steadily from the first trimester, peaks about weeks 28-32, and plateaus.
Plasma volumeUp 40-50%Risen about 10 weeks onward.
Red cell massUp about 20-30%Smaller rise than plasma.
Cardiac outputUp 30-50%See below.
Heart rateUp 10-20 beats/minPeaks in the 3rd trimester.
Stroke volumeUpDominates early; heart rate dominates later.
Systemic vascular resistanceDown 20-50%Oestrogen/progesterone/NO and the low-resistance placental bed.
Blood pressureSlight fallNadir in mid-2nd trimester, returns to baseline near term.
Pulse pressureWidenedBecause diastolic pressure falls more.
Sources: Creasy & Resnik's, Cardiovascular Adaptations; Barash's Table 41-1, p. 3475; Tintinalli's.

Details

  • Cardiac output rises in the first weeks, is 30-45% above non-pregnant by week 20, and stays there until term. It peaks between weeks 20 and 26. Early on the increase comes from stroke volume, later from heart rate. - Creasy & Resnik's
  • Mechanisms of hypervolaemia: steroid hormones, raised plasma renin activity and aldosterone, and possibly hPL and atrial natriuretic peptide. Hypervolaemia also occurs in trophoblastic disease, so a fetus is not essential. - Creasy & Resnik's
  • Placenta acts partly as an arteriovenous shunt, and generalised arteriolar dilatation (probably oestrogen-mediated) lowers vascular resistance. - Creasy & Resnik's
  • Clinical consequence: the hypervolaemia hides blood loss. A pregnant woman may lose 30-35% of her blood volume before showing signs of shock. - Tintinalli's
  • Supine hypotension syndrome: from 20 weeks onward, the gravid uterus compresses the inferior vena cava when she lies supine. Venous return and cardiac output fall, causing hypotension, pallor, sweating and dizziness. Managed by left lateral tilt. - Tintinalli's; Creasy & Resnik's
  • Labour: pain raises sympathetic tone, and each contraction pushes about 300-500 mL of blood from the uterus into the circulation (std). After placental separation there is autotransfusion of at least 500 mL. This can precipitate pulmonary oedema in a woman with severe heart disease. - Creasy & Resnik's
  • Heart and clinical signs:
    • The apex beat is displaced upward and to the left.
    • Systolic ejection murmurs and a loud third heart sound are common. (std)
    • A small silent pericardial effusion is common on echo.
    • The chest X-ray shows a slightly enlarged cardiac silhouette.
  • ECG: the mean QRS axis may shift to the left from the raised diaphragm, and to the right in late pregnancy. Minor ST and T-wave changes occur. - Creasy & Resnik's
  • Peripheral: venous pressure in the legs rises, giving oedema, varicose veins and haemorrhoids. Twin pregnancy raises cardiac output a further 20%. - Creasy & Resnik's

4. Haematological changes

  • Physiological (dilutional) anaemia: plasma volume rises more than red cell mass, so Hb falls to about 11-12 g/dL, with haematocrit around 33%. Iron treatment corrects true deficiency. - Creasy & Resnik's; Barash's. The WHO/ICMR cut-off for anaemia in pregnancy is Hb below 11 g/dL. (std)
  • Iron: the total requirement is about 1000 mg, with absorption rising in the 2nd and 3rd trimesters. (std)
  • WBC: rises to 9,000-15,000/mm³, and may reach 25,000 in labour (neutrophil leucocytosis). (std)
  • Platelets: unchanged or mildly reduced (gestational thrombocytopenia). (std)
  • ESR: raised, so it is not useful in pregnancy. (std)
  • Coagulation: a hypercoagulable state.
    • Fibrinogen and factor VII rise markedly, and fibrinogen may double.
    • Factors II and V stay about the same, while XI and XIII fall.
    • Antithrombin III and protein S fall.
    • Fibrinolytic activity is reduced.
    • PT and aPTT shorten slightly.
    • Net result: protection against haemorrhage at delivery, but a higher risk of venous thromboembolism. - Miller's Anesthesia; Barash's
  • Plasma proteins: total protein and albumin fall (albumin about 3 g/dL), which affects drug binding and lowers colloid osmotic pressure. (std)
  • Serum cholinesterase falls 20-30%. - Barash's

5. Respiratory system

ParameterChange
Tidal volumeUp about 45%
Minute ventilationUp about 50%
Alveolar ventilationUp about 70%
Respiratory rateSmall increase
Functional residual capacityDown 20-30% (residual volume down about 25%, expiratory reserve volume down about 20%)
Total lung capacityMinimal decrease
FEV1, FVC, FEV1/FVCUnchanged
Vital capacityUnchanged (std)
Closing capacityUnchanged
O₂ consumptionUp about 20%
CO₂ productionUp about 35%
Source: Barash's, pp. 3474-3475.
  • Mechanism: progesterone drives ventilation and causes bronchodilation. It sensitises the respiratory centre to CO₂.
  • Blood gases (std): PaCO₂ falls to about 28-32 mmHg and PaO₂ rises to about 100-105 mmHg. This is a compensated respiratory alkalosis, with bicarbonate falling to about 18-21 mEq/L and pH around 7.40-7.45.
  • Hyperventilation of pregnancy gives a sense of breathlessness (physiological dyspnoea) that is common in the 3rd trimester.
  • Thoracic cage: the diaphragm rises by up to 4 cm. The ribs flare, and the AP and transverse chest diameters increase, so total lung capacity is little changed. Breathing becomes more thoracic. - Tintinalli's; Barash's
  • Upper airway: capillary engorgement and oedema of nasal, oropharyngeal and laryngeal mucosa. The Mallampati score tends to rise, so airway management is harder and nasal tubes bleed easily. - Barash's. Rhinitis of pregnancy is common.
  • Anaesthetic relevance: lower FRC with higher O₂ use means rapid desaturation during apnoea.

6. Renal and urinary system

  • GFR and renal plasma flow: both rise. RPF increases sharply in early pregnancy (about 60-80% above baseline at midgestation) and GFR rises about 40-50%, peaking at midgestation. Late in pregnancy RPF falls back toward baseline while GFR stays high, so the filtration fraction rises. - Barash's; Brenner & Rector's; Harrison's
  • Lab consequences: serum creatinine falls (to about 0.5 mg/dL), urea falls (to about 9 mg/dL) and uric acid falls. A "normal" creatinine of 1.0 mg/dL may mean renal impairment in pregnancy. - Morgan & Mikhail's; Barash's
  • Glycosuria: the tubular threshold for glucose (and amino acids) falls, so mild glycosuria can occur in normal pregnancy. - Morgan & Mikhail's
  • Ureters and pelvis: dilatation of the calyces, pelvis and ureters (physiological hydronephrosis and hydroureter), more on the right. It arises from progesterone-induced smooth-muscle relaxation and compression by the uterus at the pelvic brim. (std) This predisposes to urinary stasis, pyelonephritis and asymptomatic bacteriuria.
  • Bladder: frequency of micturition in the 1st and 3rd trimesters. The bladder is displaced anteriorly into the abdomen in the third trimester, so it is more vulnerable to injury. - Tintinalli's. Stress incontinence is common.
  • Fluid balance: sodium and water retention. Total body water increases by about 6-8 L, and the osmotic threshold for thirst and ADH release is reset about 10 mOsm/kg lower. (std) Dependent oedema is common.
  • RAAS: activated, yet blood pressure stays normal because vasopressor responsiveness to angiotensin II is reduced. (std)

7. Gastrointestinal system

  • Mouth: gingival hyperaemia and gingivitis (epulis in some), and ptyalism. (std)
  • Nausea and vomiting in early pregnancy are linked to hCG, with oestrogen and progesterone implicated in the dysmotility. - Yamada's; std
  • Lower oesophageal sphincter: reduced tone from progesterone and the cephalad displacement of the stomach, so heartburn and reflux are common. - Creasy & Resnik's; Miller's Anesthesia
  • Gastric emptying: Barash's states it is not significantly delayed in non-labouring patients but is delayed in labour (and with opioids). Tintinalli's states it is delayed. The two sources differ, so for exams the usual safe teaching is that gastric acid secretion and tone fall, with a high aspiration risk in labour and general anaesthesia.
  • Intestines: reduced motility from progesterone, giving constipation. Haemorrhoids result from straining and venous pressure. The small bowel and appendix are pushed upward. - Tintinalli's
  • Gallbladder: reduced motility, larger fasting volume and reduced ejection fraction, with more lithogenic bile, so gallstones are more common. - Yamada's
  • Liver: no major structural change. Serum alkaline phosphatase rises (placental origin), while albumin and transaminases are normal to lower. (std)

8. Endocrine changes

  • Placenta as an endocrine organ: hCG peaks at about 8-10 weeks (maintains the corpus luteum). Oestrogen and progesterone rise steadily, hPL (placental lactogen) rises to term, and relaxin comes from the corpus luteum. (std)
  • Pituitary (anterior): it can double or triple in size from lactotroph hyperplasia, with volume up 40% in the 2nd trimester, 75% in the 3rd and a maximum of 120% postpartum. Prolactin rises about 10-fold across gestation. LH and FSH fall. Placental GH replaces pituitary GH as pregnancy advances. ACTH rises 2-4 fold, and total cortisol rises about threefold by term. - Creasy & Resnik's. Sheehan's syndrome is a danger if the enlarged gland is injured by postpartum haemorrhage. (std)
  • Thyroid (std):
    • Mild thyroid enlargement is common.
    • TBG rises with oestrogen, so total T4 and T3 rise.
    • Free T4 stays normal.
    • hCG has weak TSH activity, so TSH may fall in the first trimester.
    • Iodine requirement increases.
  • Parathyroid and calcium (std): total calcium falls because albumin falls, but ionised calcium stays normal. Calcium absorption rises, and PTH is normal or slightly raised. Calcium demand is about 1-1.2 g/day.
  • Adrenal (std): aldosterone, cortisol and deoxycorticosterone rise.
  • Pancreas and glucose metabolism (std): pregnancy is diabetogenic. hPL, cortisol, progesterone and prolactin cause insulin resistance, so fasting glucose is lower and postprandial glucose is higher. Hence the screen for gestational diabetes at 24-28 weeks.

9. Metabolic changes and weight gain

  • Weight gain: about 10-12 kg in total in Indian women, with a recommended range based on pre-pregnancy BMI. (std) Typical breakdown at term (std, approximate): fetus 3.3 kg, placenta 0.6 kg, liquor 0.8 kg, uterus 0.9 kg, breasts 0.4 kg, blood 1.2 kg, extracellular fluid 1.5 kg, maternal fat 3-4 kg.
  • BMR: rises by about 15-20%. An extra 300 kcal per day is advised in the 2nd and 3rd trimesters (ICMR advises roughly 350 kcal). (std)
  • Carbohydrate: see insulin resistance above. Glucose is spared for the fetus ("accelerated starvation").
  • Protein: positive nitrogen balance, with about 925 g of protein deposited in total. (std) Extra protein is needed (ICMR adds about 8-23 g/day depending on the trimester).
  • Fat: lipid stores build up in the first half; in the second half lipolysis rises and triglycerides, cholesterol and free fatty acids increase.
  • Minerals: requirement of iron (about 1 g in total), calcium, zinc and iodine rise.
  • Vitamins: folic acid requirement rises (prevents neural tube defects). Vitamin B12, C and D needs also rise.
  • Water: about 6-8 L of retained water. (std)

10. Skin, musculoskeletal and other changes

  • Skin:
    • Striae gravidarum arise from rupture of subcuticular elastic fibres as the abdomen distends. - Essentials of Forensic Medicine
    • Linea nigra, darkening of the nipples and areolae, and chloasma/melasma (the "mask of pregnancy") from raised MSH and oestrogen. (std)
    • Spider naevi and palmar erythema from oestrogen. (std)
    • Increased sweating and sebaceous activity. Hair enters telogen late in pregnancy and sheds after delivery (telogen effluvium). (std)
  • Musculoskeletal:
    • Relaxin and progesterone loosen the pelvic joints and ligaments, with widening of the symphysis pubis and sacroiliac joints.
    • Lumbar lordosis develops to compensate for the forward-shifted centre of gravity ("pride of pregnancy" posture), causing backache.
    • Gait changes give the waddling gait. (std)
    • The rectus abdominis muscles may separate (diastasis recti).
  • Nervous system (std): carpal tunnel syndrome, meralgia paraesthetica, sleep disturbance, mood changes and emotional lability.
  • Eyes (std): corneal thickness increases, intraocular pressure falls, and contact lenses may fit poorly.
  • Immune system (std): maternal immunity is modulated toward tolerance of the fetus, with a shift toward Th2 and reduced cell-mediated immunity. This is why some infections (for example influenza, malaria, hepatitis E) are more severe in pregnancy.
  • Posture and temperature (std): mean body temperature rises slightly from progesterone.

11. Changes by trimester (quick summary)

SystemFirst trimesterSecondThird
UterusPelvic organ, soft isthmus (Hegar's)Abdominal organ, umbilicus by 20 wkXiphisternum by 36 wk
Blood volumeStarts to riseRapid risePlateau from about 30-32 wk
BPFallsNadirReturns to baseline
Cardiac outputRapid risePeaks 20-26 wkStable, can fall supine
GFRRises quicklyPeaksRemains high
SymptomsNausea, frequency, fatigue"Feels well", quickeningDyspnoea, oedema, heartburn, backache

12. Clinical correlates and exam points

  1. Signs of pregnancy that come from these changes (std): Hegar's (6th week), Goodell's (cervical softening), Chadwick's/Jacquemier's (bluish vagina, 4th week), Osiander's (fornix pulsation), Braxton Hicks (from the 2nd trimester), and Palmer's sign (rhythmic uterine contractions in the first trimester).
  2. Why pregnant women with anaemia or heart disease decompensate: a 40-50% increase in blood volume, peaking at 28-32 weeks, in labour and just after delivery. The highest-risk periods are 28-32 weeks, labour, and the immediate postpartum period.
  3. Why shock appears late after haemorrhage: hypervolaemia (30-35% loss before signs). - Tintinalli's
  4. Why the creatinine reference range is lower: increased GFR.
  5. Why UTIs are common and ascend more often: ureteric dilatation and urinary stasis (progesterone and mechanical compression).
  6. Why heartburn occurs: reduced LES tone and displaced stomach. - Creasy & Resnik's
  7. Why DVT is more likely: hypercoagulability, venous stasis and pelvic vein compression.
  8. Why a pregnant woman is at risk of aspiration and a difficult airway at anaesthesia. - Barash's; Miller's
  9. Why a glucose challenge is routinely done: the diabetogenic state of pregnancy.
  10. Why pregnancy is a state of "physiological anaemia": dilution, since plasma volume rises more than red cell mass.

13. Short mnemonics (std)

  • Blood changes: "Plasma goes up most, cells follow, Hb comes down."
  • Pregnancy signs: "Hegar softens, Goodell loosens, Chadwick bluens."
  • Cardiac output: "Up 40, peak by 20-26 weeks, flat to term."

14. Recent evidence check

A PubMed search of systematic reviews from the last two years returned only gait and birth-intervention reviews. Nothing on core maternal physiology conflicts with these notes.
I can also turn this into a one-page revision table, or add a section on puerperal reversal of these changes. And again, if you send me text from Mudaliar or Shaw's, I'll fold in their specific points.
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