Recurrent Miscarriage Treatment in Ahmedabad

Responsible for 50–60% of individual miscarriages and 30–40% of RPL cases

What happens: During fertilisation, errors can occur in how chromosomes are divided between cells. An embryo with an abnormal number of chromosomes (aneuploidy) — too many or too few — cannot develop into a viable pregnancy. The body recognises this and expels the pregnancy, typically before 10 weeks. This is not a failure of the mother’s body. It is the body working correctly — rejecting an embryo that cannot survive. The tragedy is that it looks and feels like a miscarriage.

Why it causes RPL: Aneuploidy rate increases with maternal age — rapidly after 35 and dramatically after 38. However, some younger women have eggs with inherently higher error rates due to ovarian reserve issues, genetic conditions, or paternal sperm DNA fragmentation. If the underlying egg or sperm quality issue is not addressed, each new embryo carries the same chromosomal risk.

Investigation — Parental Karyotyping: Blood test for both partners. Identifies rare but important structural chromosomal abnormalities (translocations, inversions) that consistently produce unbalanced embryos. Found in approximately 2–5% of RPL couples — but critical when present because it changes the entire treatment strategy.

Investigation — Products of Conception (POC) Genetic Testing: When a miscarriage occurs, Dr. Shah requests that the products of conception (when accessible) are sent for chromosomal analysis — FISH or microarray. If the lost pregnancy was chromosomally abnormal, this is direct evidence that aneuploidy was the cause. This result transforms the next treatment decision.

The Solution — PGT-A (Preimplantation Genetic Testing for Aneuploidies): IVF with PGT-A is the single most powerful intervention for chromosomally-driven RPL. Embryos are created via IVF, cultured to blastocyst stage (day 5), biopsied for genetic analysis, and only chromosomally NORMAL (euploid) embryos are transferred. The miscarriage rate after PGT-A transfer of a euploid embryo drops to approximately 5–10% — compared to 20–40% in unscreened transfers. For a couple who has lost 3 or 4 pregnancies, transferring a confirmed-normal embryo changes the clinical picture entirely.

Sperm DNA Fragmentation: Often overlooked in RPL investigation. High levels of sperm DNA damage produce embryos that fertilise normally but carry hidden genetic damage that causes early arrest or miscarriage after initial implantation. Dr. Shah includes DFI (DNA Fragmentation Index) testing in all RPL workups — particularly when previous losses occurred after a heartbeat was confirmed.

Found in approximately 10–15% of RPL couples — often completely reversible with surgery

Uterine Septum — The Most Common Structural Cause: A uterine septum is a band of avascular (non-blood-supply) fibrous tissue that divides the uterine cavity. An embryo that implants on the septum cannot establish normal placentation — because the septum has no blood supply. The pregnancy implants, a heartbeat may develop, and then at 8–12 weeks the blood supply fails and the pregnancy is lost. This pattern — loss after a confirmed heartbeat — is strongly suggestive of a septal or vascular anatomical cause. Diagnosed by 3D TVS or hysteroscopy. Treatment: hysteroscopic metroplasty (septum incision) — day procedure, no incisions.

Uterine Polyps and Submucosal Fibroids: Both cause mechanical interference with implantation and placentation. A polyp or submucosal fibroid at the implantation site creates an abnormal blood supply environment — the embryo may implant but cannot develop normal placental vascular connections. Both are treated by hysteroscopic removal — the same day-care procedure.

Intrauterine Adhesions (Asherman’s Syndrome): Scarring within the uterine cavity — most commonly caused by prior D&C procedures (including previous miscarriage management), infection, or surgery. Adhesions physically block the cavity and reduce endometrial blood flow. Diagnosed on hysteroscopy. Treated by hysteroscopic adhesiolysis.

Arcuate Uterus vs Bicornuate Uterus: Minor uterine shape variants (arcuate uterus) are likely not clinically significant for miscarriage. Major variants (bicornuate, unicornuate, didelphys) are associated with RPL. Diagnosed on 3D TVS or MRI. Management depends on severity — most do not require surgical intervention.

Investigation and Treatment: All anatomical causes are assessed by: 3D TVS + SIS (saline infusion sonography) + diagnostic/operative hysteroscopy. Where hysteroscopy identifies a correctable lesion — septum, polyp, fibroid, adhesions — operative removal is performed in the same sitting.

Antiphospholipid Syndrome found in 15–20% of RPL cases — fully treatable

Antiphospholipid Syndrome (APS) — The Critical Diagnosis: APS is an autoimmune condition in which the body produces antibodies (anticardiolipin, anti-beta-2 glycoprotein, lupus anticoagulant) that trigger microscopic clotting within the placental blood vessels. The placenta normally forms a rich vascular network during weeks 8–12 — this is precisely when APS-related placental thrombosis occurs, causing sudden loss of blood supply to the developing pregnancy. The miscarriage occurs at 8–14 weeks, typically after a confirmed heartbeat. APS is found in 15–20% of women with RPL and is one of the most important treatable causes of late first-trimester and second-trimester pregnancy loss.

Other Inherited Thrombophilias: Factor V Leiden mutation, Prothrombin gene mutation, MTHFR variants, Protein C and Protein S deficiency — these inherited clotting tendencies impair placental microvascular development at critical stages. Their contribution to RPL is debated in the literature — Dr. Shah interprets results in clinical context, not in isolation.

Investigation — Thrombophilia Screen: Full panel: anticardiolipin antibodies (IgG and IgM), anti-beta-2 glycoprotein antibodies, lupus anticoagulant — tested twice, 12 weeks apart (APS requires two positive tests to confirm). Plus: Factor V Leiden PCR, Prothrombin gene, Protein C, Protein S, MTHFR mutation testing.

NK Cell Testing — A Note on Controversy: Elevated natural killer (NK) cells in the endometrium have been proposed as a cause of RPL in some clinics — and expensive immunological treatments offered on this basis. Dr. Shah’s approach: the evidence for NK cell testing and treatment in RPL remains inconclusive per current ESHRE guidelines. He does not recommend or offer this testing routinely — patients deserve evidence-based clarity, not expensive tests of uncertain value.

The Treatment — LMWH + Low-Dose Aspirin Protocol: Confirmed APS or significant thrombophilia is treated with: Low Molecular Weight Heparin (LMWH — Clexane/Enoxaparin) — a subcutaneous injection started with a positive pregnancy test and continued through 34 weeks gestation, plus low-dose aspirin (75–100mg) started pre-conception. With this protocol, live birth rates in APS patients improve from approximately 10% (untreated) to 70–80%. This is one of the most dramatic treatment success stories in reproductive medicine.

Thyroid, progesterone, insulin — all measurable, all correctable

Thyroid Dysfunction — The Most Commonly Missed Hormonal Cause: Subclinical hypothyroidism — a mildly elevated TSH (2.5–4.5 mIU/L) with normal T3/T4 — is associated with a 2–3 fold increase in miscarriage risk and is found in a significant proportion of RPL patients. Overt hypothyroidism (TSH >4.5) and Hashimoto’s thyroiditis (positive anti-TPO antibodies) carry even higher risk. The key: standard ‘normal’ thyroid range is too broad for pregnancy — Dr. Shah targets TSH <2.5 mIU/L in all fertility patients and treats subclinical hypothyroidism with low-dose levothyroxine before attempting conception.

Progesterone Deficiency — The Luteal Phase Problem: Progesterone is the hormone that maintains the uterine lining after ovulation and supports implantation and early placentation. Inadequate progesterone levels — luteal phase defect — can result in early pregnancy loss before the placenta takes over progesterone production at 10–12 weeks (the luteal-placental shift). Diagnosed by mid-luteal progesterone levels or progesterone levels in early pregnancy. Treated with progesterone supplementation (vaginal pessaries/gel or intramuscular injection) from positive pregnancy test through 12–16 weeks.

Insulin Resistance and PCOS: Women with PCOS and insulin resistance have elevated LH levels, androgens, and abnormal glucose metabolism — all of which impair embryo quality and endometrial receptivity. Metformin therapy in insulin-resistant women with PCOS has been shown in multiple studies to reduce miscarriage rates in both natural and IVF cycles.

Poorly Controlled Diabetes: Maternal hyperglycaemia (high blood sugar) in early pregnancy is associated with significantly elevated miscarriage rates and congenital abnormalities. Pre-conception HbA1c target: <6.5% (48 mmol/mol). Dr. Shah requests fasting glucose and HbA1c in all RPL workups, particularly in women with PCOS, obesity, or family history of diabetes.

Investigation — Hormonal Panel for RPL: TSH + Anti-TPO antibodies. Fasting glucose + HbA1c. AMH + Day 3 FSH/LH + oestradiol (ovarian reserve). Mid-luteal progesterone (Day 21 of natural cycle or equivalent). Prolactin. All tests available as a single coordinated panel.