Friday, October 9, 2026

HYPEEREMESIS GRAVIDARUM

Hyperemesis Gravidarum — Assessment, Treatment & Warning Signs
Swaraj Hospital logo
SWARAJ HOSPITAL & RESEARCH INSTITUTE
BOLANGIR, ODISHA  •  OBSTETRICS & GYNAECOLOGY CLINICAL PATHWAY SERIES
Clinician Reference Infographic

Hyperemesis Gravidarum — Assessment, Treatment & Warning Signs

Hyperemesis gravidarum is severe, persistent vomiting in early pregnancy that causes dehydration, weight loss and electrolyte disturbance. The pathway is to grade it, exclude other causes, replace fluids and thiamine, and escalate antiemetics in steps — while watching for the dangerous complication, Wernicke's encephalopathy.

Nausea and vomiting of pregnancy (NVP) affects 70–80% of pregnancies; it starts around 4–6 weeks, peaks at about 9 weeks, and settles by 16–20 weeks in most

Hyperemesis gravidarum (HG) is the severe end — about 0.3–3% of pregnancies: persistent vomiting with weight loss over 5% of pre-pregnancy weight, dehydration (ketonuria) and electrolyte disturbance

About 1 in 10 women with HG continue to vomit until delivery

HG is not “just morning sickness”. It is a serious, treatable condition that can cause Wernicke's encephalopathy, loss of work and mental-health harm — treat early and take the woman seriously.
🧬 WHY IT HAPPENS — AND WHO IS AT RISK
Mechanisms

hCG peaks at 9–12 weeks, matching the timing of symptoms

GDF15 — a hormone made by the placenta that acts on the brainstem; maternal sensitivity to it decides severity

Oestrogen, progesterone and slowed gastric emptying add to the load

Transient thyroid stimulation in many (see work-up)

Risk Factors

Previous HG or a mother or sister with HG

Multiple pregnancy and molar pregnancy (high hCG)

Nulliparity, young age, obesity or a history of migraine and motion sickness

Smoking lowers the risk

Typical HG: starts before 9 weeks, comes without fever, severe pain or headache, and with a normal abdomen

Think again if: vomiting begins after 9–10 weeks, or there is abdominal pain, fever, diarrhoea, headache, neck stiffness, or urinary symptoms

Gastrointestinal: gastroenteritis, hepatitis, pancreatitis, cholecystitis, appendicitis, peptic ulcer

Urinary and metabolic: UTI or pyelonephritis, diabetic ketoacidosis, hyperthyroidism, Addison's disease

Pregnancy-related: multiple pregnancy and molar pregnancy — an early ultrasound is part of the work-up (see our GTD guide)

📏 ASSESS SEVERITY — THE PUQE SCORE
In the last 12 hours12345
Hours of nauseaNone≤ 12–34–6> 6
Episodes of vomitingNone1–23–45–6≥ 7
Episodes of retchingNone1–23–45–6≥ 7
Mild: total score ≤ 6
Moderate: total score 7–12
Severe: total score ≥ 13 — consider admission
Also record: weight against pre-pregnancy weight, hydration, pulse, blood pressure, and ketones on urine dipstick. Repeat at every visit.
1
Urine ketones and urinalysis with culture
2
Urea, creatinine and electrolytes — look for low potassium, low sodium and a metabolic alkalosis; add magnesium, calcium and phosphate if admitted
3
Full blood count, glucose, and liver function (mildly raised transaminases are common)
4
TSH and free T4 — frequently shows transient hyperthyroidism; treat only if clinical thyrotoxicosis is present
5
Ultrasound to confirm viability and exclude molar or multiple pregnancy
6
Amylase or lipase, and blood gas if there is pain or severe illness
📈 STEPWISE MEDICAL TREATMENT
Step 1 — LifestyleSmall, frequent, bland or cold meals; avoid triggers such as strong smells; ginger and P6 acupressure may help; take iron-containing vitamins at night or pause them
Step 2 — First-line drugsPyridoxine (vitamin B6) 10–25 mg three to four times daily, with or without doxylamine; or an antihistamine: promethazine 12.5–25 mg every 4–6 h, or cyclizine 50 mg three times daily
Step 3 — Second-line drugsMetoclopramide 5–10 mg three times daily, or prochlorperazine; ondansetron 4–8 mg every 8 h if still vomiting (small possible first-trimester risk; may cause constipation or QT prolongation)
Step 4 — RefractoryCorticosteroids (hydrocortisone 100 mg IV twice daily, then oral prednisolone tapered) only after 10 weeks; other options include mirtazapine or gabapentin, with specialist advice

Combine drugs from different classes when one fails, and use the oral, rectal, or parenteral route that the woman can keep down

Add a PPI or H2 blocker for reflux; treat constipation, which makes nausea worse

Doses are typical adult doses. Always check local formulary and the individual's QT risk, other drugs, and kidney function.

Admit if: PUQE ≥ 13, persistent vomiting with ketonuria despite oral antiemetics, weight loss over 5%, electrolyte disturbance, an inability to keep down fluids or medicines, or a coexisting condition such as diabetes

Day-care or ambulatory IV therapy works for many moderate cases and avoids full admission

IV fluidsIsotonic saline or Hartmann's with potassium added to correct deficits; monitor sodium and avoid rapid correction
ThiamineGive thiamine before any dextrose-containing fluid — 100 mg IV daily during admission, or oral thiamine 100 mg daily when vomiting settles
ElectrolytesReplace potassium, magnesium and phosphate; correct hyponatraemia slowly to avoid osmotic demyelination
ThromboprophylaxisLMWH for admitted women, with compression stockings and early mobilisation, because dehydration and immobility raise VTE risk
NutritionRefractory cases: nasogastric or nasojejunal feeding, or parenteral nutrition as a last resort; watch for refeeding syndrome
🚨 WERNICKE'S ENCEPHALOPATHY — A MEDICAL EMERGENCY
Suspect it in any woman with prolonged vomiting who develops confusion, drowsiness, unsteady gait, double vision, nystagmus, or ophthalmoplegia — the full triad is rare
Treat at once with IV thiamine, 200–500 mg three times daily, before any glucose; do not wait for the scan or the blood test
Replace magnesium, correct the electrolytes, and seek urgent neurology and critical-care advice
Untreated, it leaves permanent memory loss (Korsakoff syndrome) or death — and the fetus is at risk
⚠️ COMPLICATIONS
Maternal

Wernicke's encephalopathy (thiamine deficiency)

Hypokalaemia, hyponatraemia, and metabolic alkalosis

Mallory–Weiss tear, and rarely oesophageal rupture

VTE, vitamin K deficiency with bleeding, and refeeding syndrome

Depression, anxiety and traumatic stress

Fetal / Neonatal

Weight loss over 5% is linked to low birth weight and preterm birth

Most babies are healthy when HG is treated well

Folate, iron, and vitamin deficiencies need prevention

Prolonged severe cases need growth scans

Recognise the burden: HG can cause isolation, job loss, and thoughts of termination; ask about mood and offer psychological support

Reassure: antiemetics at standard doses have wide safety data, and untreated HG carries more risk than most treatments

Most women improve by 16–20 weeks, though some need treatment to term

Recurrence is common (often more than half of later pregnancies) — offer pre-emptive antiemetics and early review in the next pregnancy, ideally starting before symptoms begin

Termination of pregnancy is considered only in severe, refractory cases after full counselling and specialist input

⛔ WHAT NOT TO DO

Do not dismiss her as having “morning sickness” — early treatment prevents admission

Do not give dextrose before thiamine in a vomiting woman

Do not correct sodium quickly, and do not give steroids before 10 weeks

Do not treat transient biochemical hyperthyroidism with antithyroid drugs unless there is true thyrotoxicosis

Do not withhold safe antiemetics from fear of birth defects — discuss the evidence

Memory Aid

HYPER

Five habits for every woman with severe vomiting in pregnancy.
H
Hydrate — isotonic IV fluids with potassium, and replace electrolytes
Y
Yield to a stepwise antiemetic plan — B6 and antihistamines first, then add and escalate
P
PUQE score, weight, and urine ketones — score her at every visit
E
Exclude other causes and examine for molar or multiple pregnancy
R
Replace thiamine before dextrose, and suspect Wernicke's in any confusion
Remember: early, adequate treatment shortens the illness, protects the brain, and spares the mother a long admission.

Immulology in Pregnancy

Immunology of Normal Pregnancy
Swaraj Hospital logo
SWARAJ HOSPITAL & RESEARCH INSTITUTE
BOLANGIR, ODISHA  •  OBSTETRICS & GYNAECOLOGY CLINICAL PATHWAY SERIES
Clinician Reference Infographic

Immunology of Normal Pregnancy — How the Fetus Escapes Rejection

A baby is half foreign to its mother, yet pregnancy normally proceeds without rejection. The explanation is active, regulated tolerance at the placental interface — combined with a mother whose general defences stay on guard. Understanding it explains pre-eclampsia, recurrent loss, Rh disease, autoimmune flares and infection risk.

The fetus carries 50% paternal antigens, so it is a semi-allograft inside the mother — yet it is not rejected. Medawar posed this paradox in 1953

The answer is not that pregnancy switches off the maternal immune system. Immunity is modulated: tolerance is built locally at the placental interface, and the mother's systemic defences stay largely intact

The tolerance rests on three ideas: a trophoblast with little to recognise, a decidua full of regulatory cells, and molecular brakes on T cells and complement

Pregnancy is immunologically active, not suppressed. That is why it can still reject a virus, a Rh-positive red cell, or — when tolerance fails — the pregnancy itself.
🧬 THE MATERNAL–FETAL INTERFACE — WHO IS IN THE DECIDUA?
Uterine NK cells (about 70%)

CD56-bright, CD16-negative — different from blood NK cells

Not killers here: they secrete VEGF, PlGF and IL-10

Help remodel spiral arteries and guide trophoblast invasion

Decidual Macrophages (20–25%)

Mostly M2-like (anti-inflammatory) phenotype

Clear apoptotic cells and tissue debris

Make IL-10 and support tissue remodelling

T Cells (3–10%)

Regulatory T cells (CD4⁺ CD25⁺ FOXP3⁺) expand in pregnancy and suppress anti-fetal responses

CD8 cells are held in a restrained state

Dendritic Cells & Others

Few DCs — and immature, tolerogenic

Very few B cells

Decidual stromal cells shape the cytokine climate

In early pregnancy, about a third of decidual cells are leukocytes — the decidua is an immune organ built for tolerance, not for rejection.

The syncytiotrophoblast, bathed directly in maternal blood, carries no classical HLA molecules (no class I or II) — there is nothing for T cells to recognise

Extravillous trophoblast (EVT), which invades the decidua and touches maternal cells, switches off HLA-A, HLA-B and class II, but expresses a special set: HLA-C, HLA-E and HLA-G

Trophoblast typeHLA-A / BHLA-CHLA-EHLA-GClass II
Syncytiotrophoblast (villous)✗✗✗✗✗
Extravillous trophoblast✗✓✓✓✗

HLA-G binds inhibitory receptors (ILT2, ILT4) on NK cells and T cells — a “don't attack” signal; HLA-E engages NKG2A; HLA-C talks to KIR receptors on uterine NK cells

KIR/HLA-C match matters: a mother with the inhibitory KIR AA genotype carrying a fetus with HLA-C2 has a higher risk of pre-eclampsia, growth restriction and recurrent loss — trophoblast invasion is too shallow

🛡️ MOLECULAR BRAKES ON THE MATERNAL IMMUNE SYSTEM
1
IDO (indoleamine 2,3-dioxygenase) breaks down tryptophan and starves activated T cells
2
PD-L1 on trophoblast engages PD-1 on T cells and switches them off
3
Fas ligand triggers apoptosis of activated maternal T cells at the interface
4
Complement regulators CD55 (DAF), CD46 (MCP) and CD59 protect trophoblast from complement attack
5
Hormones: hCG draws Tregs to the decidua; progesterone acts through PIBF to favour tolerance
6
Galectins and trophoblast exosomes carry anti-inflammatory signals into the maternal circulation
Phase 1 — ImplantationPro-inflammatory. Controlled inflammation helps the embryo attach, invade and repair the endometrium; macrophages, NK cells and cytokines (IL-1, IL-6, TNF-α) rise. Too little or too much impairs implantation
Phase 2 — GrowthAnti-inflammatory. From the end of the first trimester, Tregs and M2 macrophages dominate with IL-10 and TGF-β; this is the calm phase that supports fetal growth
Phase 3 — LabourPro-inflammatory again. Neutrophils and macrophages enter the myometrium and cervix; IL-1β, IL-6, IL-8 and prostaglandins drive contractions, cervical ripening and membrane rupture
The old Th1 versus Th2 idea is too simple. Pregnancy is not just a Th2 state — the immune balance changes with the stage of pregnancy. Infection or inflammation in phase 2 can trigger preterm labour.
🌡️ SYSTEMIC IMMUNITY — WHAT CHANGES IN THE MOTHER
Innate Immunity — Up

Neutrophils and monocytes are activated

Physiological leukocytosis: WBC about 10,000–16,000/µL, higher in labour

Complement and acute-phase proteins rise

Cell-Mediated Immunity — Down

Th1 responses are reduced and Treg activity is increased

Weaker defence against intracellular pathogens

Shifts back to normal after delivery

Humoral Immunity — Preserved

B-cell function is maintained and vaccines work

Total IgG falls slightly through haemodilution

IgG is actively transferred to the fetus

Postpartum Rebound

Immune function returns to baseline within weeks

Autoimmune flares often follow delivery (RA, MS, thyroid disease)

Postpartum thyroiditis fits this pattern

🦠 WHY SOME INFECTIONS HIT HARDER IN PREGNANCY
Influenza and COVID-19 — higher risk of pneumonia, ICU admission and preterm birth
Varicella — severe pneumonia in the mother; hepatitis E — fulminant liver failure, especially in the third trimester
Malaria — more severe disease, placental malaria and anaemia; listeriosis — intracellular infection, with stillbirth risk
Low threshold to test and treat early, and to vaccinate with inactivated vaccines (influenza, Tdap, COVID-19) — live vaccines are avoided

Improve in pregnancy (Th1 / cell-mediated): rheumatoid arthritis (about 60% improve), multiple sclerosis (relapses fall, especially in the third trimester), and Graves' disease

May worsen (antibody-mediated): systemic lupus erythematosus, particularly with active disease at conception

Postpartum flare is common in nearly all of them — plan follow-up and drug review before and after delivery

Plan pregnancy for quiet disease, and check antibodies (anti-Ro/La, antiphospholipid) that affect the fetus

🚚 ANTIBODY TRANSFER ACROSS THE PLACENTA

Only IgG crosses, using the neonatal Fc receptor (FcRn) on the syncytiotrophoblast — IgM, IgA and IgE do not cross

Transfer begins at about 13 weeks, rises steeply after 28 weeks, and fetal IgG may exceed maternal levels at term; the order of efficiency is IgG1 > IgG4 > IgG3 > IgG2

Preterm babies receive less antibody — they are more vulnerable to infection

Clinical use: Tdap at 27–36 weeks of each pregnancy and influenza vaccination in any trimester protect the newborn; raised IgM in cord blood suggests intrauterine infection, because maternal IgM cannot cross

Harm: the same pathway carries anti-D antibodies (Rh disease), anti-HPA-1a (fetal thrombocytopenia), and anti-Ro/La (congenital heart block)

Pre-eclampsia

Poor trophoblast invasion; KIR AA + HLA-C2 risk

Fewer Tregs, more inflammatory cytokines and antiangiogenic factors

Higher risk with a new partner or short sperm exposure

Miscarriage & RPL

Reduced Tregs and altered uNK function in some cases

Antiphospholipid syndrome — an immune cause with proven treatment

See our RPL and Miscarriage guides

Alloimmunisation

Rh disease: anti-D from fetomaternal bleed

FNAIT: anti-HPA-1a destroys fetal platelets; first pregnancy may be affected

Prevention: anti-D immunoglobulin

Preterm Labour

Infection or inflammation triggers phase 3 early

Chorioamnionitis and bacterial vaginosis are classic drivers

Immune activation precedes cervical change

🧫 FETAL MICROCHIMERISM

Fetal cells enter the mother from early pregnancy and can persist for decades; maternal cells also enter the fetus

They may help wound repair and tissue maintenance, but are also being studied in autoimmune disease such as scleroderma

A reminder that the maternal–fetal border is a controlled exchange, not a wall

“Pregnancy is immunosuppressed” — wrong; it is immune-modulated, and infections can be severe

Routine NK-cell, cytokine or HLA testing in recurrent loss — no proven value and not recommended

IVIG, steroids, intralipid or paternal lymphocyte immunisation for unexplained loss — not supported by trials

Withholding inactivated vaccines in pregnancy — they protect mother and baby

Memory Aid

SHIELD

Six ways the fetus escapes rejection.
S
Syncytiotrophoblast barrier — no classical HLA to recognise
H
HLA-G, -C and -E on extravillous trophoblast — inhibitory signals to NK and T cells
I
IDO and PD-L1 — brakes that switch off activated T cells
E
Expanded Tregs — FOXP3⁺ regulatory cells under the influence of hCG and progesterone
L
Local uNK cells and M2 macrophages — remodel arteries rather than attack
D
Decidual defences — FasL and complement regulators (CD55, CD46, CD59)
Remember: when tolerance is too weak the result is pre-eclampsia, loss or alloimmune disease; when it is too strong, the mother is exposed to infection. Normal pregnancy sits between the two.

Thursday, October 8, 2026

Gestational Trophoblastic Disease

Gestational Trophoblastic Disease — Molar Pregnancy to GTN
Swaraj Hospital logo
SWARAJ HOSPITAL & RESEARCH INSTITUTE
BOLANGIR, ODISHA  •  OBSTETRICS & GYNAECOLOGY CLINICAL PATHWAY SERIES
Clinician Reference Infographic

Gestational Trophoblastic Disease — Molar Pregnancy to GTN

Gestational trophoblastic disease ranges from a benign hydatidiform mole to a highly curable cancer (gestational trophoblastic neoplasia). The pathway is simple but unforgiving: recognise it, evacuate it safely, follow hCG to normal, and treat promptly if hCG plateaus or rises.

Gestational trophoblastic disease (GTD) is a group of conditions arising from abnormal proliferation of placental trophoblast, all of which make hCG

Benign (premalignant): complete hydatidiform mole and partial hydatidiform mole

Gestational trophoblastic neoplasia (GTN): invasive mole, choriocarcinoma, placental site trophoblastic tumour (PSTT) and epithelioid trophoblastic tumour (ETT)

Commoner in Asia than in Western countries (roughly 1 in 500 pregnancies against 1 in 1000 or fewer); risk factors are maternal age under 15 or over 35, a previous molar pregnancy, and prior miscarriage

GTN is among the most curable cancers — with timely diagnosis and chemotherapy, cure rates exceed 90–95%, and fertility is usually preserved. The key is reliable hCG follow-up.
🔬 COMPLETE VERSUS PARTIAL MOLE
Complete Mole

46,XX (rarely 46,XY), entirely paternal in origin — no maternal DNA

No fetus or embryonic tissue; diffuse swelling of all villi

hCG usually very high (often above 100,000 IU/L)

p57 negative on immunostaining

15–20% go on to need chemotherapy for GTN

Partial Mole

Triploid (69,XXY or 69,XXX): two paternal and one maternal set

Abnormal fetal or embryonic parts, with focal villous swelling

hCG often only modestly raised

p57 positive (maternal gene present)

1–5% develop GTN — much lower, but not zero

Vaginal bleeding in early pregnancy (the commonest symptom) — sometimes passage of grape-like vesicles

Uterus larger than dates, hyperemesis, and bilateral theca-lutein ovarian cysts from very high hCG

Systemic effects: early-onset pre-eclampsia (before 20 weeks), hyperthyroidism (hCG acts on the TSH receptor), anaemia

Ultrasound: complete mole shows a heterogeneous mass with many small cystic spaces — the “snowstorm” or “cluster of grapes” pattern and no fetus; partial mole shows a thickened cystic placenta with an abnormal or growth-restricted fetus

Many moles are now found on routine early scans, before classic features appear. Any miscarriage tissue should be sent for histology — a molar pregnancy can look like a simple missed miscarriage. See our Miscarriage guide.
🚨 STABILISE FIRST — COMPLICATIONS TO LOOK FOR BEFORE EVACUATION
Hyperthyroidism or thyroid storm: tachycardia, tremor, fever — give a beta-blocker, and treat before anaesthesia
Severe pre-eclampsia or eclampsia in the first half of pregnancy, with blood-pressure control and magnesium sulphate
Heavy bleeding, anaemia, or coagulopathy — cross-match blood before evacuation
Acute respiratory distress from trophoblastic embolisation or high-output failure — can follow evacuation of a large mole
📋 WORK-UP ON DIAGNOSIS
1
Quantitative serum hCG — the baseline for all follow-up
2
Blood group and Rh type, full blood count, clotting screen, and liver and renal function
3
Thyroid function (TSH, free T4) if clinical or biochemical features of hyperthyroidism
4
Chest X-ray for baseline lung metastases; further imaging only if GTN or symptoms

Suction evacuation under ultrasound guidance is the treatment of choice, whatever the uterine size — even in women who want future fertility

Start oxytocin at or just after evacuation, once the cervix is dilated and the uterus is being emptied, to limit bleeding

Avoid medical evacuation with prostaglandins or misoprostol and avoid hysterotomy — these raise the risk of bleeding and persistent disease

Hysterectomy can be offered if she has completed her family or has uncontrollable bleeding, though it does not remove the risk of GTN

Rh-negative women: give anti-D immunoglobulin after evacuation

Send all evacuated tissue for histology (and p57 staining if needed)

📈 FOLLOW-UP AFTER EVACUATION — hCG SURVEILLANCE
Weekly hCGStarting after evacuation, until 3 consecutive normal results (ACOG-style protocol) — local protocols vary
Monthly hCGFor about 3–6 months after normalisation in complete mole; for partial mole, a shorter course is usually enough
RegisterEnrol in the national or hospital trophoblastic disease registry where available — it supports long-term follow-up and early treatment

Contraception is essential until hCG surveillance is complete — a new pregnancy would confound hCG interpretation

Combined oral contraceptives are acceptable; avoid an IUCD until hCG has normalised (perforation risk with an invasive mole)

Follow serum hCG, not urine tests alone. A plateau or rise in hCG is the signal for GTN, and every missed follow-up visit delays treatment.
Plateau: hCG within 10% across 4 measurements over 3 weeks (days 1, 7, 14, 21)
Rise: hCG up by more than 10% across 3 weekly measurements over 2 weeks
Persistence: detectable hCG more than 6 months after evacuation
Histological choriocarcinoma, or metastases found on imaging (lung, vagina, brain, liver)
Once GTN is diagnosed: chest CT (or X-ray), pelvic ultrasound with Doppler or MRI; add brain MRI/CT and abdominal imaging if lung metastases or high-risk disease. Biopsy of metastatic lesions is dangerous — avoid.
🗂️ STAGING AND RISK SCORING (FIGO / WHO)
Anatomical Stage

I: disease confined to the uterus

II: spread to adnexa or vagina (genital structures)

III: lung metastases, with or without genital involvement

IV: other metastatic sites — brain, liver, kidney, GI tract

Risk Group (Score)

0–6: low risk

≥ 7: high risk

Score is written after the stage, e.g. stage III:5

Higher scores mean greater chance of resistance to single-agent therapy

Prognostic factor0124
Age (years)< 40≥ 40——
Antecedent pregnancyMoleAbortionTerm—
Interval from index pregnancy (months)< 44 – < 77 – 12> 12
Pre-treatment hCG (IU/L)< 10³10³ – < 10⁴10⁴ – 10⁵> 10⁵
Largest tumour size, incl. uterus< 3 cm3 – < 5 cm≥ 5 cm—
Site of metastasesLungSpleen, kidneyGI tractBrain, liver
Number of metastases01 – 45 – 8> 8
Previous failed chemotherapy——Single drug≥ 2 drugs
Low Risk (score 0–6)

Single-agent chemotherapy: methotrexate (weekly IM, or the 8-day methotrexate–folinic acid regimen) or pulsed actinomycin D

Continue for 2–3 cycles after hCG first normalises (consolidation)

If resistant: switch to actinomycin D or move to multi-agent therapy

Score 5–6 has more resistance to methotrexate — consider an upfront alternative

High Risk (score ≥ 7)

EMA-CO multi-agent regimen: etoposide, methotrexate, actinomycin D, cyclophosphamide, vincristine

Continue until hCG is normal, then 2–3 further cycles

Brain metastases need higher-dose methotrexate with intrathecal therapy ± radiotherapy

Refer to a specialist trophoblastic centre

PSTT and ETT are rare and relatively chemo-resistant, with low hCG — hysterectomy is the primary treatment for non-metastatic disease; multi-agent therapy is used if metastatic

Hysterectomy is also considered in chemo-resistant disease or uncontrolled haemorrhage once childbearing is complete

Doses and schedules follow the oncology protocol and body-surface area; with cure rates this high, treatment belongs in an experienced centre.
🌱 AFTER TREATMENT — PROGNOSIS & FUTURE PREGNANCY

Cure rates: close to 100% for low-risk disease and about 90% or more for high-risk disease

hCG monthly for 12 months after normalisation in GTN; avoid pregnancy for 12 months after chemotherapy ends

Recurrence risk of a mole in a future pregnancy is about 1–2% — raise awareness, and offer an early ultrasound in every later pregnancy

hCG 6–8 weeks after the end of any later pregnancy, and send the placenta for histology

Fertility is usually preserved; most women go on to have healthy babies

Memory Aid

MOLE

The four steps that protect a woman with a molar pregnancy.
M
Make the diagnosis — scan, hCG, histology, and p57 where needed
O
Optimise before evacuation — treat thyroid disease, pre-eclampsia, anaemia, and cross-match blood
L
Lift out the mole with suction evacuation — avoid prostaglandins and hysterotomy
E
Ensure follow-up — weekly hCG to normal, reliable contraception, and a registry
Remember: hCG is the tumour marker. A woman who is followed reliably with hCG can be cured of GTN almost every time — a missed follow-up is the real danger.

Wednesday, October 7, 2026

Doppler in Obstetrics — Vessels, Waveforms & Clinical Action

Doppler in Obstetrics — Vessels, Waveforms & Clinical Action
Swaraj Hospital logo
SWARAJ HOSPITAL & RESEARCH INSTITUTE
BOLANGIR, ODISHA  •  OBSTETRICS & GYNAECOLOGY CLINICAL PATHWAY SERIES
Clinician Reference Infographic

Doppler in Obstetrics — Vessels, Waveforms & Clinical Action

Doppler ultrasound measures blood-flow velocity waveforms in maternal and fetal vessels. It shows how well the placenta is working and how the fetus is adapting to stress. It is a targeted test for high-risk pregnancies (growth restriction, hypertension, alloimmunisation, twins) — it is not a routine screen for low-risk women, and it never replaces CTG, growth scans or amniotic fluid assessment.

Suspected FGR / SGA — estimated fetal weight or abdominal circumference below the 10th centile

Hypertensive disorders — pre-eclampsia, chronic hypertension, or high uterine artery resistance at screening

Red-cell alloimmunisation or suspected fetal anaemia — MCA peak systolic velocity (see our Rh isoimmunization guide)

Twins — selective growth restriction, twin-to-twin transfusion syndrome, TAPS

Other triggers: reduced fetal movements, oligohydramnios, previous stillbirth or severe early-onset pre-eclampsia

Not for routine low-risk screening — universal third-trimester Doppler has not improved outcomes in low-risk women. Follow the ALARA principle and avoid routine spectral Doppler in the first trimester.
📐 READING THE WAVEFORM — THE INDICES

S/D ratio = peak systolic ÷ end-diastolic velocity. RI = (S − D) ÷ S.

PI (pulsatility index) = (S − D) ÷ mean velocity — the most useful index, because it still works when end-diastolic flow is absent or reversed

Compare against gestation-specific centiles — normal values fall as pregnancy advances, so one fixed number does not fit all weeks

Resistance is lower in a healthy placenta: the more diastolic flow, the healthier the downstream bed

Uterine Artery (maternal)

Reflects trophoblast invasion and spiral artery remodelling

Normal: early-diastolic notch disappears by about 24–26 weeks

Raised mean PI or persistent notch → higher risk of pre-eclampsia and FGR

Umbilical Artery (placental)

Reflects placental resistance — the main vessel for FGR surveillance

Measure in a free loop of cord, with no fetal breathing

Raised PI → AEDF → REDF as placental disease worsens

Middle Cerebral Artery (brain)

Normal fetal brain has high resistance

Low PI = brain-sparing (blood redirected to the brain under hypoxia)

PSV > 1.5 MoM suggests moderate–severe fetal anaemia

Ductus Venosus (venous)

Shows how the fetal heart is coping — an late sign of compromise

Normal: forward flow throughout the cardiac cycle

Absent or reversed a-wave = cardiac decompensation

📈 UMBILICAL ARTERY — THE FOUR PATTERNS
Umbilical artery Doppler waveforms: normal, raised resistance, absent end-diastolic flow, reversed end-diastolic flow
Schematic spectral waveforms. Above the line = forward flow; below the line = reversed flow in diastole.
Normal — continuous forward diastolic flow, PI within centile range
Raised PI (> 95th centile) — placental resistance rising; increase surveillance
AEDF — no forward flow in diastole; significant placental insufficiency
REDF — flow reverses in diastole; highest perinatal mortality risk
Early-onset FGR (before 32 weeks)
Normal UA DopplerRepeat about weekly (often twice weekly if the PI is raised); watch the fetal growth rate
AEDFCloser surveillance (CTG, DV Doppler); consider delivery by about 32–34 weeks if stable
REDFConsider delivery at about 30–32 weeks, earlier if DV or CTG deteriorates
DV a-wave absent/reversed, or abnormal CTG short-term variationDeliver — indicates imminent fetal compromise
Late-onset FGR (after 32 weeks)

UA Doppler is often normal even in a compromised fetus — a normal UA does not reassure on its own

Use MCA PI and the cerebroplacental ratio (CPR = MCA PI ÷ UA PI): a low CPR (below the 5th centile, or < 1) signals redistribution and higher risk of adverse outcome

Consider delivery at about 37 weeks in FGR with abnormal CPR or MCA; timing is individualised

Before delivery under 34 weeks: give antenatal corticosteroids, and magnesium sulphate for neuroprotection when delivery is expected before 32 weeks. See our ACS guide.
🚨 DOPPLER RED FLAGS — ESCALATE THE SAME DAY
Reversed end-diastolic flow in the umbilical artery
Absent or reversed a-wave in the ductus venosus, or pulsatile umbilical vein flow
MCA peak systolic velocity above 1.5 MoM (suspected fetal anaemia) — arrange fetal medicine review for possible intrauterine transfusion
Any abnormal Doppler together with a reduced-variability or decelerating CTG
🔬 MCA PSV FOR FETAL ANAEMIA — THE TECHNIQUE

Start from about 18 weeks in at-risk pregnancies; repeat every 1–2 weeks

Sample the proximal third of the MCA, near its origin from the circle of Willis

Keep the insonation angle as close to 0° as possible; take the highest velocity from several traces

Values are given as multiples of the median (MoM) for gestation; > 1.5 MoM → cordocentesis and transfusion planning

Accuracy falls after about 35 weeks — false positives rise, so interpret with clinical context

1
Record during fetal quiescence — no breathing movements, no fetal body movement
2
Keep the insonation angle below 30° (0° for MCA PSV)
3
Use low wall filter, appropriate gain, and the smallest sample volume that covers the vessel
4
Use minimal probe pressure — pressure on the fetal head can change MCA values
5
Take 3 or more similar consecutive waveforms and average them
Memory Aid

DOPPLER

A checklist for every Doppler request, from indication to action.
D
Define the indication — who is this scan for, and why?
O
Optimise settings — quiet fetus, low angle, low wall filter
P
Pick the right vessel — UA, MCA, DV, or uterine artery
P
PI against gestation-specific centiles
L
Look at trends — serial readings tell more than a single value
E
Examine alongside CTG, growth and liquor volume
R
Respond by gestation — steroids, surveillance, or delivery
Remember: a normal Doppler in a late-onset growth-restricted fetus is not the end of surveillance — it only means one pathway is still normal.

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