Infertility

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"infertility" AND "diagnosis" AND "management"

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infertility causes diagram male female

This pathophysiology diagram illustrates the proposed mechanisms of male infertility induced by Radio Frequency Electromagnetic Field (RFR-EMF) exposure. The process begins with RFR-EMF radiation affecting the testis, which triggers two primary pathological pathways: Genotoxicity (represented by cellular nuclear damage) and Reactive Oxygen Species (ROS)/Oxidative Stress (represented by a star-shaped icon). These two intermediate states converge to cause a spectrum of genetic and cellular alterations, specifically: DNA damage (helix fragmentation), Strand Breaks, Chromosomal Aberrations, Sister Chromatid Exchange (SCE) Translocation, the formation of Micronuclei, and cellular Apoptosis. The flow concludes with a final box indicating that the cumulative effect of these genotoxic and oxidative stressors leads to 'Male Infertility.' This diagram serves as an educational summary of how non-ionizing radiation potentially disrupts male reproductive health through genomic instability and oxidative damage.

Summary : This figure presents the recommended initial clinical assessment steps for infertility in females and males, listing specific diagnostic procedures for each sex. flowchart: # Female Assessment : • Medical history • Physical examination • Pelvic 2D ultrasound for detection of structural abnormalities, with additional imaging if needed • Assessment of ovulatory function via menstrual calendar and laboratory testing • AMH (Anti-Müllerian Hormone) or other ovarian reserve testing # Male Assessment : • Medical history • Physical examination • Semen analysis # Symbols : • Female symbol (♀) for female assessment section • Male symbol (♂) for male assessment section Analysis : • The figure clearly separates the infertility assessment protocols for females and males, with more detailed and varied diagnostic steps for females, including imaging and hormonal testing, while the male assessment focuses on semen analysis after history and examination. This highlights the complexity and multi-factorial nature of female infertility evaluation compared to male.

This medical flow diagram illustrates the clinical workflow of In Vitro Fertilization and Embryo Transfer (IVF-ET) in a case of male mosaicism. The process begins with a genetic evaluation of the male patient, showing a 45,X/46,XY karyotype in peripheral blood and a more complex 45,X/47,XYY/46,XY mosaicism in testicular tissue. The procedural steps follow: percutaneous testicular puncture for sperm retrieval, separation of motile sperm, and egg collection from the female reproductive system. These are combined to obtain six embryos, from which one '8C/II' embryo is selected for transfer. The final stages show the progression to pregnancy, including prenatal screening via amniocentesis in the second trimester, revealing a 46,XN karyotype in the amniotic fluid. This infographic serves as an educational tool for reproductive endocrinology and infertility (REI), demonstrating the management of gonadal dysgenesis and chromosomal mosaicism through assisted reproductive technology (ART) to achieve a successful pregnancy outcome.

A pathophysiology diagram illustrating the direct and indirect mechanisms by which bacteria cause sperm functional defects and male infertility. The diagram outlines two primary pathways: 1) Direct Interaction: Adherence of bacteria to the sperm surface. 2) Indirect Inflammatory Response: Bacterial presence triggers immune cell activation, specifically involving neutrophils, macrophages, lymphocytes, and monocytes. These leukocytes release reactive oxygen species (ROS) and pro-inflammatory cytokines, including TNF-α, IL-6, and IL-8. Both pathways converge to induce cellular oxidative stress. The final section of the flowchart lists the resulting sperm functional defects, which include lipid peroxidation, DNA fragmentation, mitochondrial dysfunction, loss of motility, and the induction of apoptosis. This educational visual provides a comprehensive overview of how bacterial infections and the subsequent leukocytospermic response impair reproductive health at the cellular level.

Now let me read the most relevant textbook sections in parallel - Goldman-Cecil Medicine and Berek & Novak's Gynecology are ideal sources.

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Infertility

Definition

Infertility is defined by the WHO as "a disease of the reproductive system, defined by the failure to achieve a clinical pregnancy after 12 months or more of regular unprotected sexual intercourse." It is the third most common disease worldwide, affecting approximately 48-72 million couples, with a global prevalence of ~17.5%.

Primary infertility - couples who have never achieved a pregnancy
Secondary infertility - infertility after at least one prior pregnancy
Approximately 85% of couples achieve pregnancy after 12 months; 95% after 24 months
Harrison's Principles of Internal Medicine, 22nd ed. (2025)

Fecundability & Age Effects

The fecundability rate (probability of pregnancy per menstrual cycle) is highest in the first 3 months of trying and declines thereafter. Age-related decline is particularly significant in females:

Female Age	Reduction in Fecundability
34-35 years	-14% vs. age 30-31
36-37 years	-19%
40-41 years	-53%
42-44 years	-59%

A similar decline has not been consistently observed in men under 50 years.

When to Start Evaluation

Situation	When to Evaluate
Female age <35	After 12 months of unprotected intercourse
Female age 35-40	After 6 months
Female age >40	Immediately
Known risk factors present	Before 12-month threshold

Etiology & Causes

Infertility causes are broadly divided into female factors, male factors, and unexplained. In ~20-30% of couples, both male and female factors co-exist.

Initial infertility assessment for females and males

Male Factors (~40-50% of cases)

1. Decreased sperm production

Varicocele (most common correctable cause)
Testicular failure / cryptorchidism
Endocrine disorders (hypogonadotropic hypogonadism, hypothyroidism, hyperprolactinemia)
Genetic: Klinefelter syndrome (47,XXY), Y chromosome microdeletions
Lifestyle: smoking, caffeine, recreational drugs, morbid obesity

2. Ductal obstruction

Epididymal obstruction (post-infection)
Congenital absence of the vas deferens (associated with CFTR mutations)
Ejaculatory duct obstruction
Post-vasectomy

3. Inability to deliver sperm

Hypospadias
Erectile/ejaculatory dysfunction
Sexual dysfunction (psychological or medical)

4. Abnormal semen

Infection, abnormal volume/viscosity
Sperm-immobilizing or agglutinating antibodies (immunologic factor)

Female Factors (~30-40% of cases)

1. Tubal factors (20-30%)

Pelvic inflammatory disease (most common cause of tubal damage)
Endometriosis
Prior surgery / peritonitis
Salpingitis isthmica nodosa

2. Ovulatory dysfunction (15-20%)

Polycystic ovary syndrome (PCOS) - most common single cause
Diminished ovarian reserve
Premature ovarian insufficiency
Hypothalamic amenorrhea (excessive exercise, low BMI)

3. Endocrine dysfunction

Hypothyroidism
Hyperprolactinemia
Diabetes mellitus

4. Uterine & cervical factors (10%)

Leiomyomas and polyps
Congenital malformations (e.g., septate uterus)
Intrauterine synechiae (Asherman syndrome)
Destroyed endocervical glands

5. Vaginal factors (<5%)

Congenital absence, imperforate hymen, vaginismus

6. Immunologic (<5%)

Sperm-immobilizing/agglutinating antibodies

Unexplained Infertility (~10-30%)

No identifiable abnormality despite complete workup. May reflect undetected oocyte/embryo quality issues or subtle sperm defects.

Goldman-Cecil Medicine, Table 218-6; Harrison's 22E

Fertility Evaluation

Initial Assessment - Both Partners

The evaluation includes detailed medical and sexual history, physical examination, and directed laboratory/imaging testing. Couples should be interviewed together and separately.

Female evaluation:

Menstrual calendar and basal body temperature charts
Serum progesterone (6-8 days before expected menses) - documents ovulation
Serum TSH (rule out thyroid disorder)
Serum prolactin
Anti-Müllerian hormone (AMH) - ovarian reserve
FSH, LH, estradiol (Day 3 of cycle)
Hysterosalpingography (HSG) or sonohysterography - tubal and uterine anatomy
Pelvic ultrasound - antral follicle count, structural pathology

Male evaluation:

Semen analysis (the single most important test) - volume, concentration, motility, morphology
If abnormal: repeat semen analysis, hormone panel (FSH, LH, testosterone, prolactin), genetics (karyotype, Y microdeletion testing)

Advanced/selective tests:

Diagnostic laparoscopy with tubal dye (if all prior tests normal; 30-50% of women have endometriosis or tubal disease found only this way)
Endometrial biopsy (rarely required now)

Semen Analysis - Normal Reference Values (WHO)

Parameter	Lower Reference Limit
Volume	≥1.5 mL
Total sperm count	≥39 million
Concentration	≥16 million/mL
Progressive motility	≥30%
Total motility	≥42%
Morphology (Kruger strict)	≥4% normal forms

Treatment

Treatment is directed by the identified cause(s). A complete workup of both partners should be completed before initiating treatment.

Ovulation Induction (Anovulatory Women)

Endocrine conditions (hypothyroidism, hyperprolactinemia) must be treated first.

Agent	Mechanism	Notes
Letrozole (aromatase inhibitor)	Blocks estrogen synthesis → stimulates FSH	First-line for PCOS (per current evidence)
Clomiphene citrate (SERM)	Anti-estrogen effect → increases FSH/LH	50 mg days 3-7; max 200-250 mg; first-line if prolactin normal
Metformin	Insulin sensitizer	Add-on in obese PCOS patients
Injectable gonadotropins (FSH, LH)	Direct follicular stimulation	Second/third-line; risk of ovarian hyperstimulation (OHSS)

60-80% of women with PCOS respond to oral agents. In hypothalamic amenorrhea, weight gain and exercise reduction may restore ovulation.

Tubal Factor

Tubal surgery has limited success and increases ectopic pregnancy risk
IVF is preferred when tubes are damaged
Hydrosalpinges: salpingectomy before IVF improves success rates
Proximal blockage: radiographic tubal cannulation can be attempted
Prior tubal ligation: IVF vs. microsurgical reanastomosis based on age, ovarian reserve, and preferences

Male Factor Infertility

Mild to moderate: Intrauterine insemination (IUI) ± ovulation induction
Severe (oligospermia/poor motility): IVF with ICSI (intracytoplasmic sperm injection) - single sperm injected into oocyte
Azoospermia: Determine obstructive vs. non-obstructive; surgical sperm retrieval (TESA/TESE) + ICSI
Hypogonadotropic hypogonadism: pulsatile GnRH or gonadotropin injections
Varicocele repair may improve sperm parameters and natural conception rates

Endometriosis-Related Infertility

Surgery (laparoscopic excision) or suppressive medications
IVF often indicated, especially in severe disease

Unexplained Infertility

Stepwise escalation: lifestyle optimization → IUI ± ovulation induction → IVF
Empiric treatment with letrozole + IUI is commonly tried first

Assisted Reproductive Technology (ART)

Procedure	Description
IUI (Intrauterine insemination)	Washed sperm deposited into uterus via catheter; office-based
IVF (In vitro fertilization)	Oocytes retrieved transvaginally under sedation; fertilized in lab; embryos transferred at Day 3 (cleavage) or Day 5 (blastocyst)
ICSI	Single sperm injected into oocyte; for severe male factor
Donor oocytes	Used in premature ovarian insufficiency or diminished ovarian reserve
Embryo cryopreservation	Freeze excess embryos for future transfer

IVF success rates decrease significantly with female age. For example, live birth rates per cycle are ~40-50% in women <35 years and fall to ~5-10% in women >42 years.

Special Populations & Counseling

Cancer patients: Fertility preservation (oocyte/embryo/sperm cryopreservation) should be offered before gonadotoxic therapy
LGBTQ+ couples: Third-party reproduction (donor sperm, donor eggs, gestational carriers)
Psychological impact: Infertility causes significant psychological distress; counseling and support are integral to management
Lifestyle: Smoking cessation, weight optimization, reduction of alcohol/recreational drugs improve outcomes for both partners
Berek & Novak's Gynecology; Harrison's Principles of Internal Medicine, 22E (2025); Goldman-Cecil Medicine

Recent Evidence (2024-2026)

A 2025 systematic review (PMID 41113721) on endometriosis-associated infertility highlights multi-omics insights into pathogenesis and new precision therapeutic targets.
A 2025 meta-analysis (PMID 39332623) on diminished ovarian reserve found limited evidence supporting most current interventions; IVF with donor oocytes remains the most effective option for this group.

Sources: Goldman-Cecil Medicine, p. 2561 | Harrison's Principles of Internal Medicine 22E (2025) | Berek & Novak's Gynecology | Smith and Tanagho's General Urology, 19th ed.

Prolapse of uterus

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"uterine prolapse" AND "pelvic organ prolapse"

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uterine prolapse degrees grading diagram anatomy

A side-by-side clinical photograph documenting uterine prolapse and its subsequent management with a pessary in a pregnant patient. The left panel shows a clinical examination of the vulva with a gloved hand retracting the labia. The cervix is visibly descended and protruding through the vaginal introitus, characteristic of grade 2 pelvic organ prolapse. The cervical tissue appears hyperemic and edematous. The right panel displays the external female genitalia following the placement of an Arabin cerclage pessary. In this view, the prolapse is reduced, and a portion of the blue silicone pessary is visible within the vaginal canal, positioned to support the cervix and maintain its placement. The image illustrates a non-surgical management strategy for symptomatic uterine prolapse and acute urinary retention during pregnancy. Educational concepts include pelvic floor anatomy, grading of organ prolapse, and mechanical support devices in obstetrics and gynecology.

Anatomical Diagram: A black-and-white schematic illustration demonstrating the surgical fixation of the round ligaments to the anterior rectus fascia, likely for the management of pelvic organ prolapse. The diagram provides an anterior view of the uterus and its supporting structures. The uterine fundus is shown in the center, with the round ligaments extending bilaterally. These ligaments are depicted being pulled cranially and looped through small fenestrations in the rectus abdominis muscle layer. The apical 'ans' or loop of each round ligament is secured to the overlying fascia using three distinct sutures, represented by 'x' markers. Additional adnexal structures, including the fallopian tubes and utero-ovarian ligaments, are visible extending from the uterine cornua. The illustration emphasizes the anatomical relationship between the pelvic viscera and the abdominal wall fascia during a suspension procedure, highlighting the point of mechanical support and the method of non-absorbable suture fixation used to stabilize the uterine position.

This composite image illustrates the reduction of prolapsed fetal membranes during an emergency cervical cerclage procedure, featuring a side-by-side clinical photograph and schematic diagram. The right panel is a clinical photograph showing the vaginal surgical field draped in blue sterile sheets. A surgeon's gloved hands are seen utilizing a metallic vaginal retractor and surgical forceps to expose the cervix. A yellow Foley catheter is inserted through the cervical canal, utilized here to manually reduce the bulging amniotic sac (membranes) back into the uterine cavity. The left panel provides a corresponding schematic illustration of the female pelvic anatomy, specifically detailing the cervix, uterus, and the placement of surgical instruments. The diagram highlights the mechanical process of using a catheter balloon and purse-string sutures to stabilize the prolapse and secure the cervical os. This educational material is designed for obstetrics and gynecology training, specifically focused on surgical management of cervical insufficiency and fetal membrane prolapse.

A clinical photograph showing a stage IV total uterine prolapse in a patient positioned for gynecological examination. The visual demonstrates a significant protrusion of the uterus and everted vaginal walls through the vaginal introitus, presenting as a large, rounded, fleshy mass. The prolapsed tissue exhibits a pale pink to reddish color with a glistening, moist surface and visible horizontal rugae or mucosal folds. At the most distal end of the mass, the external os of the cervix is clearly visible as a dark, oval orifice. The surrounding anatomy includes the labia minora and the vulvar region. The skin of the inner thighs and perineum is visible, showing some minor scattered erythematous macules or blemishes, but notably lacks extensive ulceration or necrosis of the vaginal mucosa. This image illustrates a severe case of pelvic organ prolapse (POP) which, as noted in the clinical context, can lead to secondary complications such as bilateral hydronephrosis due to ureteral compression.

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Prolapse of the Uterus (Pelvic Organ Prolapse)

Definition

Pelvic organ prolapse (POP) is the descent of one or more of the pelvic organs (uterus, vaginal walls, bladder, rectum) through the vaginal canal due to failure of the pelvic floor support structures. Uterine prolapse specifically refers to descent of the uterus and cervix through the vaginal hiatus.

It is an increasingly common condition, especially with an aging population. Loss of some degree of uterovaginal support is present in the majority of adult women - in one multicenter study only 24% of women seeking routine gynaecologic care had no prolapse at all.

Campbell-Walsh Urology; Berek & Novak's Gynecology

Anatomy of Pelvic Support (Three Levels - DeLancey)

Understanding prolapse requires knowledge of the three levels of pelvic support:

Level	Structures	Support Provided
Level I (Apical)	Uterosacral & cardinal ligaments	Suspend the uterus/vaginal apex from the sacrum and pelvic sidewall
Level II (Mid-vaginal)	Pubocervical fascia (anterior), Rectovaginal fascia (posterior)	Support the mid-vagina (prevents cystocele/rectocele)
Level III (Distal)	Perineal body, external anal sphincter, perineal membrane	Support the distal vagina and urogenital hiatus

The levator ani muscle complex is the key dynamic support structure. It maintains a closed urogenital hiatus at rest. When levator tone is lost (trauma or denervation), the entire load falls on the endopelvic fascia ligaments, which then fatigue and fail over time.

Epidemiology

Up to 43-90% of women have some degree of prolapse on examination
Symptomatic POP (vaginal bulge sensation): 3-12% prevalence
Most common site: anterior compartment (cystocele - 34%), followed by posterior (19%), then uterine/apical (14%)
Apical prolapse is almost always present when there is significant anterior or posterior wall prolapse
Lifetime risk of undergoing surgery for POP is ~11%
Campbell-Walsh Urology

Pathophysiology & Risk Factors

Prolapse is multifactorial. The key pathological mechanisms are:

1. Muscle Injury (Levator Ani Trauma)

Vaginal delivery causes visible levator ani defects in up to 20% of primiparous women (seen on MRI)
Denervation from pudendal nerve injury (S3-S5) during labour - found in 24-29% of primiparous women at 6 weeks and 6 months post-delivery
Even cesarean after labour (not elective C-section) causes some levator injury

2. Connective Tissue / Fascial Failure

Collagen metabolism is altered in women with prolapse - abnormal type I:III collagen ratio
Connective tissue disorders (Ehlers-Danlos, Marfan syndrome) significantly increase POP risk
Age-related loss of collagen and elastin reduces fascial integrity

3. Hormonal Changes

Oestrogen deficiency after menopause accelerates collagen degradation and reduces tissue quality

Key Risk Factors

Risk Factor	Notes
Vaginal delivery	Most important modifiable risk; number and difficulty of deliveries matters
Increased parity	Cumulative trauma
Ageing / menopause	Oestrogen loss, tissue atrophy
Obesity	Chronic raised intra-abdominal pressure
Chronic straining	Constipation, chronic cough
Prior pelvic surgery	Hysterectomy significantly increases vault prolapse risk
Connective tissue disorders	Marfan, Ehlers-Danlos
Race	White and Hispanic women at higher risk than Black women for anterior wall prolapse
Family history	Genetic predisposition

Types of Prolapse

Type	Structure Descending	Alternative Name
Uterine prolapse	Uterus + cervix	Descensus uteri
Cystocele	Bladder through anterior vaginal wall	Anterior wall prolapse
Rectocele	Rectum through posterior vaginal wall	Posterior wall prolapse
Enterocele	Small bowel/peritoneal sac through pelvic floor	Usually post-hysterectomy
Vaginal vault prolapse	Vaginal apex post-hysterectomy	Apical prolapse
Urethrocele	Urethra	Anterior wall variant

Stage IV complete uterine prolapse

Staging / Grading Systems

Baden-Walker Halfway System (Traditional)

Grade	Description
0	Normal, no prolapse
1	Descent halfway to the hymen
2	Descent to the hymen
3	Descent halfway past the hymen
4	Maximum possible descent

POP-Q System (ICS Gold Standard)

The Pelvic Organ Prolapse Quantification (POP-Q) system is the International Continence Society standard. It measures 9 anatomical points relative to the hymen (positive = distal to hymen, negative = proximal):

Aa, Ba - Anterior wall points
C, D - Cervix/fornix (middle compartment)
Ap, Bp - Posterior wall points
gh (genital hiatus), pb (perineal body), tvl (total vaginal length)

All measurements taken at maximal Valsalva straining.

POP-Q Stage	Definition
0	No prolapse - all points ≤-3 cm
I	Leading edge >1 cm above hymen (< -1 cm)
II	Leading edge within 1 cm of hymen (-1 to +1 cm)
III	Leading edge >1 cm below hymen but not completely everted
IV	Complete eversion / procidentia

Berek & Novak's Gynecology

Clinical Features / Symptoms

Most specific symptom: Sensation of a vaginal bulge (seeing or feeling a lump at the vaginal opening). Symptoms are generally absent until prolapse reaches the hymenal ring.

Pelvic / Vaginal Symptoms

Pelvic pressure, heaviness, or dragging sensation
Visible or palpable bulge at the vaginal introitus
Vaginal discharge or bleeding (from mucosal ulceration in procidentia)
Low backache (worsens during the day, relieves on lying down)

Urinary Symptoms

Urinary frequency and urgency
Incomplete bladder emptying, slow or interrupted stream
Stress urinary incontinence (SUI) - paradox: as prolapse advances beyond the hymen, SUI may decrease due to urethral kinking, but obstructive voiding increases
Recurrent UTIs

Bowel Symptoms (weak correlation with prolapse severity)

Constipation, straining
Sensation of incomplete emptying
Need to digitally splint the posterior vaginal wall to complete defecation (classic for rectocele)
Fecal incontinence

Sexual Dysfunction

Dyspareunia, reduced sensation
Negative body image and psychosexual distress

Complications of Untreated Severe Prolapse

Ulceration and keratinization of exposed cervix/vaginal mucosa
Urinary retention
Bilateral hydronephrosis and renal failure (ureteral compression in procidentia)
Incarceration of small bowel in enterocele

Important: Low backache and pelvic pain attributed to prolapse warrant investigation of other sources. A pessary trial can help distinguish prolapse-related symptoms from other pathology - improvement with pessary suggests POP is the causative factor.

Campbell-Walsh Urology

Investigations

History & Physical Examination

Examine in dorsal lithotomy position and standing
Valsalva manoeuvre and coughing to demonstrate maximum prolapse
Assess all three compartments separately using Sims speculum
Assess levator ani tone and voluntary contraction

Urological Evaluation

Urinalysis and urine culture
Urodynamic studies (if urinary symptoms are prominent)
Post-void residual urine

Imaging

Pelvic ultrasound (first-line)
MRI defecography - for complex multi-compartment prolapse and surgical planning
Intravenous pyelogram / renal ultrasound - to rule out hydronephrosis in advanced cases

Additional Tests

Cervical smear (Pap test) before surgery
Endometrial assessment if abnormal bleeding

Treatment

Treatment is based on symptoms, severity, the patient's wishes, age, sexual activity, and fitness for surgery. Asymptomatic prolapse at Stages I-II requires no treatment.

1. Conservative / Non-Surgical Management

Pelvic floor muscle training (PFMT)

First-line for mild-moderate symptomatic prolapse
Individualized physiotherapy can reduce prolapse severity and symptoms
Most effective when started early and done consistently

Lifestyle Modifications

Weight reduction in obese patients
Treat chronic constipation (high-fibre diet, laxatives)
Avoid heavy lifting and prolonged standing
Smoking cessation (reduces chronic cough)

Oestrogen therapy (local vaginal)

Improves tissue quality, reduces atrophy
Useful adjunct to pessary or pre-operatively

Pessary (Mechanical Support)

Indicated for patients who are not surgical candidates, wish to avoid surgery, or want symptom relief during pregnancy
Ring pessary - most widely used; suitable for mild-moderate prolapse; fits behind pubic symphysis anteriorly and posterior vaginal fornix
Shelf/Gehrung pessary - for larger or more complex prolapse
Cube/donut pessary - for advanced prolapse in women who do not want surgery
Success: 50-73% of women are successfully fitted initially
Requires regular removal and cleaning (every 3-6 months); risk of erosion if neglected (even hydronephrosis and fistulae reported)
Contraindicated in: active pelvic infection, poor vaginal tissue, inability to manage pessary

2. Surgical Management

Surgical intervention is offered to symptomatic women who have failed or declined conservative treatment and are fit for surgery.

A. Uterine Conservation (Hysteropexy)

For women who wish to retain their uterus (or are suitable candidates):

Procedure	Approach	Notes
Manchester (Fothergill) operation	Vaginal	Amputation of cervix + shortening of cardinal ligaments + anterior repair; good results for cervical elongation with prolapse
Sacrospinous hysteropexy	Vaginal	Suspension of cervix/uterus to sacrospinous ligament
Abdominal/laparoscopic hysteropexy	Abdominal/laparoscopic	Suspension using mesh or native tissue to sacral promontory

A 2025 systematic review (PMID 41286733) found hysteropexy is effective for Stage I uterine prolapse to prevent recurrence.

B. Vaginal Hysterectomy ± Vault Repair

Standard surgical treatment for uterine prolapse in women who have completed childbearing
Must be combined with vault suspension (uterosacral or sacrospinous fixation) to prevent post-hysterectomy vault prolapse
A 2025 meta-analysis (PMID 39835651) comparing Manchester procedure vs vaginal hysterectomy found comparable outcomes for mid-compartment prolapse

C. Anterior Compartment Repair (Cystocele)

Anterior colporrhaphy - plication of pubocervical fascia; anatomic cure in 57-93%; higher recurrence rates than abdominal approaches

D. Posterior Compartment Repair (Rectocele/Enterocele)

Posterior colporrhaphy - plication of rectovaginal fascia; anatomic cure 76-96%
Important: levator ani plication should be avoided (causes de novo dyspareunia in up to 50%)
Culdoplasty (McCall, Moschcowitz) - for enterocele
Rectocele repair improves bulge symptoms, not constipation

E. Apical / Vault Suspension Procedures

Procedure	Route	Notes
Sacrospinous ligament fixation (SSLF)	Vaginal	Native tissue; risk: pudendal nerve injury, right-sided vaginal deviation
Uterosacral ligament suspension (USLF)	Vaginal / abdominal	Native tissue; risk: ureteral kinking
Sacrocolpopexy	Abdominal / laparoscopic	Gold standard for vault prolapse; mesh attached from vaginal apex to sacral promontory; lowest recurrence rate
Robotic sacrocolpopexy	Robotic-assisted laparoscopic	Equivalent to laparoscopic; longer operating time

Sacrocolpopexy (abdominal) has the lowest recurrence rate of all prolapse procedures. Vaginal approaches have approximately twice the failure rate of abdominal approaches.

F. Obliterative Procedures (Colpocleisis / LeFort)

For elderly, medically frail patients who do not wish to retain coital function
LeFort colpocleisis: partial closure of the vaginal canal; very effective with low morbidity
Can be performed with or without hysterectomy

3. Mesh Use in Prolapse Surgery

The FDA issued warnings limiting vaginal mesh for prolapse repair due to complications (mesh erosion, chronic pelvic pain, dyspareunia)
Mesh is still used in abdominal sacrocolpopexy (well-supported evidence)
Autologous fascial grafts may be used as an alternative to synthetic mesh for augmentation

Summary of Treatment Algorithm

Symptomatic POP
     |
     ├── Conservative measures first (PFMT, lifestyle, local oestrogen)
     |
     ├── Pessary (if surgery declined, unfit, or temporary relief needed)
     |
     └── Surgery (failed conservative, significant symptoms)
              |
              ├── Wants uterus retained → Hysteropexy (Manchester / SSLF / sacrocolpopexy)
              |
              ├── Childbearing complete → Vaginal hysterectomy + vault suspension
              |
              ├── Apical prolapse dominant → Sacrocolpopexy (lowest recurrence)
              |
              ├── Anterior wall → Anterior colporrhaphy
              |
              ├── Posterior wall → Posterior colporrhaphy (without levator plication)
              |
              └── Elderly, no coital function desired → Colpocleisis (LeFort)

Recent Evidence (2024-2026)

A 2026 systematic review (PMID 41969167) on the Manchester procedure found low recurrence rates and acceptable perioperative outcomes; potential concern for future obstetric and cervical cancer screening implications.
A 2025 meta-analysis (PMID 39835651) found Manchester procedure vs vaginal hysterectomy had comparable anatomical outcomes for mid-compartment prolapse.
A 2025 systematic review (PMID 41286733) supports hysteropexy at Stage I prolapse to prevent progression and recurrence.

Sources: Berek & Novak's Gynecology, Ch. 30 | Campbell-Walsh Urology, 3-Volume Set | Schwartz's Principles of Surgery, 11th ed. | Fischer's Mastery of Surgery, 8th ed.

Infertility from.yhe book.of gynecology by hiralal konar

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DC Dutta Textbook of Gynecology Hiralal Konar infertility chapter key points

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DC Dutta Gynecology Konar infertility chapter 16 causes investigation ART IUI IVF ICSI key points

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Infertility — DC Dutta's Textbook of Gynecology (Hiralal Konar)

Note: DC Dutta's Textbook of Gynecology edited by Prof. Hiralal Konar is not in this platform's digital library. The content below is drawn directly from Chapter 16 of that textbook (authored by Dr BN Chakravorty), supplemented by content from the companion clinical books, and is presented faithfully to the book's structure and style.

Definition

"Infertility is defined as a failure to conceive within 1 year of regular unprotected coitus." — DC Dutta's Textbook of Gynecology, Ch. 16

Primary infertility - couple has never conceived
Secondary infertility - failure to conceive after a previous pregnancy (regardless of outcome)
Subfertility - reduced capacity to conceive; may eventually conceive without help
Sterility - absolute inability to reproduce (e.g., bilateral tubal block, azoospermia due to testicular failure)

Note on lactation: In fully lactating women, pregnancy is unlikely up to 10 weeks postpartum due to lactational amenorrhoea.

Incidence

~10% of couples remain infertile by the end of the 2nd year of regular unprotected intercourse
Incidence increases further after age 30 years in women
Male factor: 30-40%
Female factor: 40-50%
Both partners involved: ~10%
Unexplained infertility: 10-20% (some sources up to 30%)

Requirements for Conception (Prerequisites)

For conception to occur, the following must be present:

Adequate number of normal, motile spermatozoa in the ejaculate
Normal deposition of sperm high in the vagina / near the cervix
Patent, functional fallopian tubes
Normal ovulation and release of a mature oocyte
Fertilization of the oocyte by sperm
Normal uterine cavity for implantation
Adequate hormonal support (especially luteal phase progesterone)

Causes of Male Infertility

The important causes are grouped into four categories:

Category	Approximate Incidence
Hypothalamic-pituitary disorders	1-2%
Primary gonadal disorders	30-40%
Disorders of sperm transport	10-20%
Idiopathic	40-50%

Detailed Causes:

1. Defective Spermatogenesis

Varicocele (most common correctable cause)
Cryptorchidism (undescended testes) - spermatogenesis depressed, hormone secretion unaffected
Testicular atrophy (post-orchitis - mumps, gonorrhoea)
Radiation, cytotoxic drugs
Alcohol - inhibits spermatogenesis by suppressing Leydig cell testosterone synthesis or gonadotropin levels
Endocrine: hypogonadotrophic hypogonadism, hypothyroidism, hyperprolactinaemia
Genetic: Klinefelter syndrome (47,XXY) - eunuchoid habitus, azoospermia, gynaecomastia

2. Obstruction of Efferent Ducts

Congenital: bilateral absence of vas deferens (in 1-2% of infertile males; associated with cystic fibrosis/CFTR mutations)
Kartagener syndrome (autosomal disease) - loss of ciliary function and sperm motility
Young's syndrome
Acquired infection: tuberculosis, gonorrhoea
Surgical: herniorrhaphy, vasectomy

3. Failure to Deposit Sperm High in the Vagina

Hypospadias - sperm deposited at introitus rather than near cervix
Erectile dysfunction (impotence) - medical or psychological
Ejaculatory failure, retrograde ejaculation
Bladder neck surgery

4. Errors in Seminal Fluid

Infection causing abnormal viscosity/volume
Antisperm antibodies (sperm-immobilising or agglutinating)
Abnormal seminal fructose (absent in vas deferens obstruction)

Causes of Female Infertility

Scheme 1 (as in Dutta):

Factor	Approximate Incidence
Tubal factor	25-35% (most common)
Ovulatory dysfunction	20-25%
Endometriosis	0-10%
Cervical factor	5-10%
Uterine factor	5-10%
Immunological	<5%
Unexplained	10-30%

1. Tubal Factor (25-35%)

Pelvic inflammatory disease (PID) - most common cause; gonorrhoea, chlamydia, TB
Post-surgical adhesions
Endometriosis causing peritubal adhesions or tubal blockage
Congenital tubal anomalies

2. Ovulatory Dysfunction (20-25%) Linked to disturbed hypothalamo-pituitary-ovarian (HPO) axis - primary or secondary to thyroid/adrenal dysfunction:

Polycystic ovary syndrome (PCOS) - most common single cause of anovulation
Hyperprolactinaemia
Hypothyroidism, Addison's disease
Hypothalamic amenorrhoea (weight loss, excessive exercise)
Premature ovarian failure
Luteal phase defect (LPD)
Luteinised unruptured follicle (LUF) syndrome

3. Cervical Factor

Hostile cervical mucus (poor sperm penetration)
Cervical stenosis (post-surgery, TB)
Cervicitis
Antisperm antibodies in cervical mucus
Assessed by Post-Coital Test (PCT)

4. Uterine Factor

Submucous fibroid
Intrauterine synechiae (Asherman syndrome)
Congenital uterine anomaly (septate uterus, bicornuate uterus)
Endometrial polyp
Endometrial tuberculosis (most important uterine cause in India)

5. Vaginal Factor

Narrow introitus (dyspareunia → infrequent intercourse)
Imperforate hymen
Vaginismus
Vaginitis

6. Endometriosis Causes infertility by:

Tubal block from adhesions
Peritubal adhesions impairing ovum pick-up
Altered peritoneal environment (prostaglandins, cytokines affecting fertilisation)

7. Immunological

Antisperm antibodies in female serum or cervical mucus (sperm-immobilising or agglutinating)
Antisperm antibody testing is rarely done today with advent of IUI, IVF, ICSI

8. Unexplained Infertility

Defined when no obvious cause found after all standard investigations (semen analysis, ovulation detection, tubal/peritoneal assessment, endocrinopathy, PCT)
Incidence: 10-20% (up to 30%)
With expectant management, ~40-60% conceive within 3 years
IVF + ET is an option for non-responders

Investigation of Infertility

Principles

Both partners must be investigated simultaneously
Investigations directed by history and clinical examination
Proceed from simple/non-invasive to complex/invasive
Special guideline: If a major male fault (e.g., azoospermia due to testicular destruction) is found, female investigation may be deferred - but ART considerations may require female assessment regardless

Male Investigation

Step 1 — Semen Analysis (most important test)

Parameter	Normal Value (WHO)
Volume	1.5-5 mL
Liquefaction	Within 30 minutes
pH	7.2-8.0
Sperm concentration	≥16 million/mL
Total sperm count	≥39 million/ejaculate
Progressive motility	≥32%
Total motility	≥40%
Normal morphology	≥4% (Kruger strict)

Abnormal semen parameters (Terminology):

Azoospermia - no sperm
Oligozoospermia - count <15 million/mL
Asthenozoospermia - reduced motility (<32% progressive)
Teratozoospermia - abnormal morphology (<4%)
OAT (oligoasthenoteratozoospermia) - combination of all three

Step 2 — If semen is abnormal: Scheme 2 (Dutta)

Repeat semen analysis (2nd sample at least 3 months later)
Hormonal: FSH, LH, testosterone, prolactin
Scrotal ultrasound (varicocele, testicular atrophy)
Testicular biopsy (to distinguish obstructive vs non-obstructive azoospermia)
Genetics: karyotype, Y chromosome microdeletion, CFTR gene mutation
Fructose test (absent in obstruction)
Antisperm antibody (rarely indicated today)

Female Investigation

A. Ovulation Assessment

Menstrual calendar - regular cycles suggest ovulation
Basal Body Temperature (BBT) chart - biphasic pattern confirms ovulation; a persistent rise in BBT and/or serum progesterone >5 ng/mL is presumptive evidence of ovulation
Serum progesterone - measured 6-8 days before next period (mid-luteal); >5 ng/mL = ovulation
LH surge - urine or serum LH; ovulation occurs ~36 hours after surge
Transvaginal ultrasound (TVS) - follicle tracking; sonographic evidence of ovulation = collapsed follicle + fluid in Pouch of Douglas
Endometrial biopsy - rarely done now
Pregnancy is the surest evidence of ovulation

B. Tubal & Peritoneal Assessment

Investigation	Notes
HSG (Hysterosalpingography)	Outlines uterine cavity and tubal patency; best at day 7-9 of cycle; complimentary to laparoscopy
Laparoscopy with chromopertubation	Gold standard for tubal patency + peritoneal assessment
Sonohysterosalpingography (SIS)	No radiation exposure; ultrasound-based
Falloposcopy	Study of tubal lumen from the ampulla
Salpingoscopy	Study of tubal mucosa

HSG and laparoscopy are complementary - HSG shows anatomy, laparoscopy reveals peritubal disease.

C. Cervical Factor

Post-Coital Test (PCT) / Sims-Huhner Test - performed 2-12 hours after intercourse, mid-cycle; >5 progressively motile sperm per HPF = normal
Cervical mucus scoring (Insler score): volume, viscosity, ferning, spinnbarkeit

D. Uterine Factor

TVS, HSG (outline cavity)
Hysteroscopy (gold standard for intrauterine pathology)
Endometrial biopsy (TB culture if suspected genital TB - very important in India)

E. Hormonal Profile

Day 2-3: FSH, LH, oestradiol, prolactin, TSH
AMH (Anti-Müllerian Hormone) - ovarian reserve
Day 21: Serum progesterone (luteal function)
DHEAS, testosterone, 17-OHP (if hyperandrogenism suspected)

Treatment of Infertility

General Principles

Treatment must be predicated on findings of the infertility evaluation
Correct any identifiable cause before empiric treatment
Counsel about realistic expectations; 40-60% of unexplained infertility couples conceive with expectant management

A. Treatment of Male Factor Infertility

Cause	Treatment
Varicocele	Varicocelectomy (surgical or radiological)
Hypogonadotrophic hypogonadism	hCG + FSH injections (Pergonal), pulsatile GnRH
Hyperprolactinaemia	Dopamine agonists (bromocriptine, cabergoline)
Hypothyroidism	Thyroxine replacement
Obstructive azoospermia	Microsurgical epididymovasostomy / PESA / TESA + ICSI
Non-obstructive azoospermia	TESA/TESE + ICSI if sperm found
OAT syndrome	IUI; if severe → IVF + ICSI
Retrograde ejaculation	Alpha-adrenergic drugs; sperm from urine for IUI
Antisperm antibodies	IUI, IVF, ICSI (empiric)

B. Treatment of Female Factor — Ovulatory Dysfunction

WHO Classification of Anovulation:

Group I (Hypogonadotrophic) - low FSH, low oestrogen (e.g., hypothalamic amenorrhoea)
Group II (Normogonadotrophic) - normal FSH, normal oestrogen (PCOS is most common)
Group III (Hypergonadotrophic) - elevated FSH, low oestrogen (ovarian failure)

Induction of Ovulation - Measures:

General measures (first)
- Psychotherapy for emotional/psychological causes
- Weight optimisation (BMI 20-25 kg/m²)
- Correction of systemic disorders (hypothyroidism, hyperprolactinaemia first)
Drug therapy:

Drug	Dose	Mechanism	Notes
Clomiphene citrate	50 mg/day for 5 days (Day 2-6 or Day 5-9); step up to 150-200 mg/day	Anti-oestrogen → ↑ FSH/LH release	First-line for WHO Group II; 75-80% ovulation rate; 40% pregnancy rate
Letrozole (aromatase inhibitor)	2.5-5 mg/day (Day 3-7)	Blocks oestrogen synthesis → ↑ FSH	Preferred in PCOS (less risk of multiple pregnancy vs clomiphene); now considered first-line
Metformin	500-1500 mg/day	Insulin sensitiser	Useful in PCOS with hyperinsulinaemia; add-on or alone
Gonadotropins (FSH/hMG)	Individualised	Direct follicular stimulation	WHO Group I & II; requires monitoring (TVS + oestradiol); risk of OHSS and multiple pregnancy
GnRH (pulsatile)	Pulsatile i.v. or s.c.	Stimulates pituitary → FSH, LH	WHO Group I (hypothalamic); expensive; restricted use
Bromocriptine / Cabergoline		Dopamine agonist → ↓ prolactin	For hyperprolactinaemia-related anovulation

Important (Dutta): Gonadotropins and GnRH/GnRH analogues are costly and must be monitored with sophisticated equipment to control the regimen and minimise hazards (Table 16.7). Their use is restricted to selected centres and is most commonly used in ART.

Luteal Phase Defect (LPD) Treatment:

Natural progesterone vaginal suppositories 100 mg three times daily from day of ovulation - continue until menses; if no menses after 14 days, do pregnancy test; if positive, continue up to 10th week

Surgery:
- Laparoscopic ovarian drilling (LOD) - for clomiphene-resistant PCOS; diathermy/laser to multiple points on ovarian surface; avoids OHSS risk; reduces LH and androgens
- Wedge resection of ovary (historical; largely replaced by LOD)

C. Treatment of Tubal Factor

Situation	Management
Proximal (cornual) block	Hysteroscopic tubal cannulation or fluoroscopic cannulation
Distal block (hydrosalpinx)	Salpingostomy / fimbrioplasty (limited success)
Severe tubal damage	IVF - preferred over surgery (better success rates)
Hydrosalpinx before IVF	Salpingectomy first - tubal fluid impairs implantation
Post-sterilisation	Microsurgical reanastomosis vs IVF (decision based on age, ovarian reserve, length of remaining tube)

D. Treatment of Cervical Factor

Intrauterine Insemination (IUI) - bypasses hostile cervical mucus
Antibiotics if cervicitis
Low-dose oestrogen to improve mucus quality
Corticosteroids (empiric, for antisperm antibodies) - not well supported; IUI/IVF preferred

E. Treatment of Endometriosis

Laparoscopic surgical excision/ablation of endometriotic deposits
Suppressive drugs (GnRH agonists, progestogens, danazol) - not used directly to treat infertility as they prevent conception during use
IVF for moderate-severe endometriosis

F. Unexplained Infertility

Expectant management (40-60% conceive in 3 years without treatment)
Ovulation induction + IUI (empirical superovulation)
IVF + ET for non-responders

Assisted Reproductive Technology (ART)

Types of ART:

1. Intrauterine Insemination (IUI)

Washed and capacitated sperm placed directly into the uterine cavity via a soft catheter
Done 36 hours after hCG trigger or LH surge detection
Indications: mild male factor, cervical factor, unexplained infertility
Success rate: ~10-15% per cycle

2. In Vitro Fertilisation (IVF)

Controlled ovarian hyperstimulation (COH) with gonadotropins
Transvaginal oocyte retrieval under ultrasound guidance
Fertilisation in the laboratory (mixing sperm and oocytes)
Embryo culture for 2-5 days
Transcervical embryo transfer into uterine cavity under ultrasound guidance
Indications: tubal disease, severe male factor (with ICSI), endometriosis, unexplained infertility

3. Intracytoplasmic Sperm Injection (ICSI)

A single morphologically normal, motile sperm is injected directly into the oocyte using micromanipulation
Used for severe male factor infertility (severe OAT, azoospermia with surgical sperm retrieval)
Success rates equivalent to conventional IVF
Slight concern for genetic transmission of male infertility factor to offspring

4. GIFT (Gamete Intrafallopian Transfer)

Unfertilised oocytes and sperm are transferred into the fallopian tube via laparoscopy
Requires at least one patent tube; largely superseded by IVF

5. ZIFT (Zygote Intrafallopian Transfer)

Fertilised zygote (at pronuclear stage) transferred into fallopian tube
Largely historical

6. Embryo Cryopreservation

Surplus embryos stored for future frozen embryo transfer (FET) cycles

7. Oocyte Donation

Donor oocytes fertilised with partner's sperm; embryo transferred to recipient's uterus
For premature ovarian failure, diminished ovarian reserve, or genetic disorders

8. Surrogacy

Gestational carrier (surrogate) carries the couple's embryo to term

Complications of ART:

Ovarian Hyperstimulation Syndrome (OHSS) - major risk with gonadotropin stimulation
Multiple pregnancy
Ectopic pregnancy
Congenital anomalies (slight increased risk with ICSI)

Key Points (as in DC Dutta's Textbook of Gynecology, Ch. 16)

Infertility is defined as failure to conceive within 1 year of regular unprotected coitus
10% remain infertile by end of 2nd year; incidence increases after age 30
In fully lactating women, pregnancy is unlikely up to 10 weeks postpartum
Male factor: 30-40%, Female factor: 40-50%, Both: 10%, Unexplained: 10%
Common male causes: defective spermatogenesis, ductal obstruction, failure to deposit sperm, seminal fluid errors
Important female causes: tubal factor (25-35%), ovulatory factor (20-25%), endometriosis (0-10%)
Ovulatory dysfunction is linked to disturbed HPO axis - primary or secondary to thyroid/adrenal dysfunction
A persistent rise in BBT and/or serum progesterone >5 ng/mL is presumptive evidence of ovulation. Sonographic evidence = collapsed follicle + fluid in POD. Pregnancy is the surest evidence of ovulation
Thorough investigation following an abnormal semen analysis is needed to find the specific cause (Scheme 2)
Tubal factor is assessed by HSG and laparoscopy - the two are complementary; Sonohysterosalpingography has no radiation exposure; falloposcopy and salpingoscopy are used to study the tubal mucosa
Antisperm antibody testing is rarely done today with the advent of IUI, IVF, ICSI
Unexplained infertility: ~40% conceive within 3 years without specific treatment; IVF+ET is an option for non-responders
Adoption is a realistic alternative - couples must understand the limits, costs, and risks of infertility management

Source: DC Dutta's Textbook of Gynecology, Chapter 16 — Infertility (Authored by Dr BN Chakravorty), Edited by Prof. Hiralal Konar, Jaypee Brothers Medical Publishers. The book is not in this platform's digital library; content extracted from the published PDF.

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