0% found this document useful (0 votes)
6 views66 pages

Infertility

Uploaded by

Lusajo Lusajo
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
6 views66 pages

Infertility

Uploaded by

Lusajo Lusajo
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
You are on page 1/ 66

INFERTILITY

Presenter: Dr. H. AYUB Mmed 2- OBGY.


OUTLINES
1. Definition of infertility
2. Causes of infertility
3. Work up investigations
4. Management of infertile
couples appropriately
5. Prognostic factors

2
DEFINITION
 Infertility is defined as an inability of couples in
highly reproductive age less than 35yrs to conceive
for 1year/ 12months despite of regular, unprotected
sexual intercourse and without using any
contraception or 6months for those above 35yrs.
 Therefore, the probability of conception depends
on the length of exposure, coital frequency, and
the age of the couple.
 The chances of conception after 1 month of
unprotected intercourse is 20 to 25%; about 50%
will be pregnant in 3months, 70% by 6 months, and
90% by 1 year.

 . 3
Types of infertility
Primary infertility
Infertility whereby there are no prior
pregnancies.
Secondary infertility
Infertility following at least one prior
conception regardless of outcome.
 Subfertility: failure to conceive after 6 months
of unprotected intercourse.
 Fecundability is the probability of achieving a
pregnancy within one menstrual cycle. For a
normal couple, this is approximately 25%.
4
Fecundability
A monthly probability of conceiving is 20 to
25%.

Inthose attempting conception,


approximately;
◦50% of women will be pregnant at 3
months,
◦75% will be pregnant at 6 months,
◦90% will be pregnant by 1 year.
5

Fertility
Reproductive age for women is generally
15-44 years.
As a woman's age increases, the incidence
of infertility also increases.
A consistent decline in fecundity after
30 to 35 years of age has been
demonstrated, with an incidence of
involuntary infertility in women at the age
of 40 ranging from approximately 33% to
64%.
Fertility is approximately halved between
37th and 45th year due to alterations in
ovulation.
6
INCIDENCE
1995 “US National Survey of Family
Growth” revealed that :
◦7% of married couples, in which the
female partner was of reproductive age,
had not achieved pregnancy after 12
months of sexual intercourse without
contraception.
◦15% of women of reproductive age
reported having received infertility
services at some point in their lives.
CAUSES OF INFERTILITY

8
CATEGORIES OF MALE INFERTILTY:
CAUSES
The causes of male infertility can be
divided into four main areas.
i. Endocrine and systemic disorders
(usually related to secondary
[hypogonadotropic] hypogonadism)
– 2 to 5%.
ii. Primary testicular defects in
spermatogenesis – 65 to 80%, of which
the majority have idiopathic
dysspermatogenesis, an isolated
defect in spermatogenesis without an
identifiable cause. 9
Categories of Male Infertility:
Causes …
iii. Sperm transport disorders – 5%.

iv. Idiopathic male infertility – 10 to 20%.


Idiopathic male infertility should be
distinguished from idiopathic
dysspermatogenesis.
Idiopathic male infertility describes an
infertile man with a normal semen
analysis and no apparent cause for
infertility, whereas infertile men with
idiopathic dysspermatogenesis have
abnormal semen analyses.
10
Male Inferility: Causes
Pre-testicularcauses:
◦Congenital or acquired diseases of:
 hypothalamus
 Pituitary
 Peripheral organs that alter the
hypothalamic-pituitary axis.
◦ This Includes:
1. Idiopathic hypogonadotropic
hypogonadism
2. Prolactinoma
3. Cushing disease
11
Male Inferility: Causes …
Primary testicular causes
◦ May be chromosomal or non-chromosomal
in nature.
A.Chromosomal abnormalities
1.Klinefelter syndrome
2.XX male (sex reversal syndrome) -crossover of
the sex-determining region (SRY) of the Y
3.XYY male
4.Mixed gonadal dysgenesis
5.Androgen receptor dysfunction
6.Bilateral anorchia (vanishing testes syndrome)
7.Down syndrome
12
Male Inferility: Causes …
 Primary testicular causes
B: Non-chromosomal testicular failure
1. Varicocele (veins coming from testicle are
dilated, or widened)
2. Cryptorchidism
3. Trauma
4. Chemotherapy
5. Radiation
6. Orchitis
7. Granulomatous diseases
8. Sickle cell diseases
9. Excessive use of alcohol, cigarettes, caffeine,
or marijuana 13
Male Inferility: Causes …
Post-testicular causes of infertility
Problems with sperm transportation
through the ductal system, either
congenital or acquired
1. Congenital blockage of the ductal
system
2. Acquired blockage of the ductal
system
3. Ejaculation issues
(Anejaculation/retrograde ejaculation)
14
Male Inferility: Causes …
Post-testicular causes of infertility …
Sperm delivery problems
◦Bilateral obstruction of epididymal
or ducts
◦Ejaculatory dysfunction e.g.
retrograde ejaculation
◦Erectile dysfunction
◦Abnormal position of urethral
orifice
Cause Azoospermia
1. Klinefelter syndrome
2. Gonadotropin deficiency
3. Hyperprolactinemia
4. Varicocele
5. Severe illness (cancer, kidney or liver failure)
6. congenital absence of the vas deferens,
7. Vasectomy
8. Testicular failure (non-obstructive azoospermia).
◦ chemotherapy,
◦ radiation,
◦ Surgery
◦ Mumps
16
FEMALE INFERTILTY: CAUSES
1. Ovulatory dysfunction
◦ Hyperprolactinemia (pituitary adenoma,
renal/hepatic failure, drugs: cimetidine,
psychotropics)
◦ Polycystic ovarian syndrome (PCOS)
◦ Systemic disease (thyroid, cushing’s syndrome)
◦ Congenital (Turners syndrome, androgen
insensitivitty syndrome, gonadal dysgenesis or
gonadotropic deficiency)
◦ Luteal phase defect
◦ Stress, poor nutrition, excessive exercise
◦ Premature ovarian failure (e.g. autoimmune
disease)
Female Infertility: Causes …
2. Tubal factors
 Blockage or impairment of the fallopian
tubes.
 Causes – PID, peritonitis, endometriosis,
surgery, congenital anomalies.
3. Uterine
i. Malformed uterus:
ii. Asherman’s syndrome (intrauterine
adhesions or synechiae)
iii.Tumours – fibroids can prevent
implantation of the embryo.
18
Female Infertility: Causes …
4. Cervical Factors
◦ Production of antibodies (in cervical mucus)
to the male's sperm.
◦ Thickness of mucus
◦ Cervical stenosis
5. Systemic diseases
 Liver dx alter metabolism of estrogen →
anovulation
 Endocrine Disorders:
 Hypo & hyperthyroidism → anovulation
 Hyperprolactinemia suppresses GnRH →
anovulation. 19
Female Infertility: Causes …
6. Drug abuse
i. Alcohol: Chronic alcoholism is related to
disorders in ovulation>
ii. Marijuana, heroin and cocaine: May disrupt
a woman's ovulation cycle.
iii. Smoking: Tobacco changes the cervical mucus, thus
affecting the way sperm reach the egg, and has adverse
affect on ovarian function and also on implantation,.
iv. Antiepileptic drugs, antidepressants,
antipsychotics, antihypertensives eg
furosamide etc, ARTs, Anti-TBs, etc

20
Female Infertility: Causes …
7. Endometriosis
May be associated with pelvic adhesions →
blockage.

8. Psychological factors
 Anxiety, stress, anorexia nervosa are a/c
excessive release of corticotropin release
hormone (by hypothalamus) which in turn
inhibits GnRH pulsatile secretion.

21
Evaluation of Infertility
 Infertility evaluation comprises eight major
elements:
 history and physical examination;
 semen analysis;
 Sperm cervical mucus interaction
(postcoital testing);
 assessment of ovarian reserve;
 tests for occurrence of ovulation;
 evaluation of tubal patency;
 detection of uterine abnormalities; and
 determination of peritoneal abnormalities.
History and Physical
Examination
Obtain an extended and complete
history from both partners and
performing a physical examination.
A sexual history should include the
◦frequency and timing of intercourse,
◦menstrual irregularity,
◦impotence,
◦dyspareunia,
◦the use of lubricants,
◦sexually transmitted diseases.
History and Physical
Examination…
Modifiable lifestyle factors that
potentially reduce fecundability should be
probed.
◦tobacco use,
◦alcohol or caffeine consumption,
◦body mass index,
◦exercise habits, and
◦Induces of stress.
Exclusion of Male Factor Infertility

The cornerstone is the semen analysis.


The semen sample should be collected
after a period of abstinence of at least 48
hours and is best evaluated within 1 hour
of ejaculation.
The sample is obtained either by sexual
intercourse with a silicone condom,
because latex condoms are spermicidal,
or by masturbation.
Endocrine evaluation
A basic endocrine evaluation of the
infertile male involves measurements of
FSH, LH, Prolactin and total
testosterone and will detect the vast
majority of clinically significant
endocrinopathies.
Testicular Biopsy
It may be diagnostic or for prognostic
purposes.
Biopsy may be performed to determine the
whether that sperm can be retrieved for
IVF with ICSI(Intracytoplasmic Sperm
Injection), results may not be all that
helpful because sperm production can be
limited to specific foci within the testes.
Diagnostic biopsy is indicated:
◦for azoospermic men with normal
testicular size,
◦one palpable vas deferens and a normal
serum FSH level, because the normal
FSH does not guarantee that
spermatogenesis is normal.
 Geneticabnormalities interfere with sperm production
or transport.
◦ mutations within the cystic fibrosis transmembrane
conductance regulator (CFTR) gene which are highly
associated with congenital bilateral absence of the
vas deferens;
◦ chromosomal anomalies resulting in testicular
dysfunction (Klinefelter syndrome; 47, XXY); and
◦ Y chromosome microdeletions at azoospermia
factor (AZF) locus at q11 associated with
abnormalities of spermatogenesis

Chromosomal evaluation
ASABs may be on the surface of sperm &
in the cervical mucus.
Spermatozoa are protected from
circulation by tight inter-Sertoli junctions.
Prevention is also aided by presence of T-
suppressor lymphocytes in the epididymis
& vas deferens.
ASABs develops in men either when the
blood-testis barrier breaks down or there
is a decrease in T-suppressor cell activity.

Antisperm Antibodies
 Antisperm antibodies can really impair the
function of healthy sperm. These antibodies
attach to your sperm, reducing motility and
making it more difficult for sperm to pass
through cervical mucus.
 Antisperm antibodies can also force sperm to
clump together, making it difficult for your
sperm to fertilize an egg
 Blood-testis barrier is breached if there is
obstruction or injury to the reproductive ducts:
 Infection: Chlamydial, gonococcal, TB etc
 vasectomy reversal
 testicular cancer
 testicular biopsy
 varicocele
Antisperm Antibodies …
 testicular torsion
Variety of tests that can detect the
presence of antisperm antibodies in the
body:
◦ Blood Tests: In women, blood tests are
commonly used to detect the antibody.
◦ Post-Coital Test: The post-coital test can
detect the presence of antisperm antibodies in
a woman's cervical mucus.
◦ Sperm Testing: In men, sperm testing is the
best way to analyze for antisperm antibodies.
The immunobead assay and the mixed
agglutination reaction test are both used.

Antisperm Antibodies …
 There are a variety of treatments available to help
couples struggling with antisperm antibodies to
conceive.
 Corticosteroids: Corticosteroids help to decrease
the production of antisperm antibodies. Unfortunately,
corticosteroids are associated with side effects,
including hipbone damage.
 Intrauterine Insemination(IUI): IUI can help
couples to overcome antisperm antibodies as it allows
sperm to bypass the cervical mucus. Fertility drugs
can also be used.
 In-Vitro Fertilization(IVF): IVF is the most
successful treatment for couples with antisperm
antibodies. This allows the sperm to be directly
injected into the egg, without having to travel throguh
the uterus and fallopian tubes.

Antisperm Antibodies …
The postcoital test (PCT) or Huhner's test
allows direct analysis of sperm and cervical
mucus interaction and provides a rough
estimate of sperm quality.
The test is done between days 12 and 14 of a
28- to 30-day menstrual cycle (after 48 hours
of abstinence) when maximum estrogen
secretion is present.
The mucus is examined within 2 to 8 hours.
Finding of 5-10 progressively motile
spermatozoa per HPF and clear acellular
mucus with a spinnbarkeit (the degree to
which the mucus stretches between two
slides) of 8 cm generally excludes a cervical
Exclusion
factor. of Cervical Factor Infertility
Interpretation of the PCT is subjective,
the validity of the test is controversial,
despite its long history of use.
Fecundity rates do not correlate directly
with number of motile sperm seen.
The most common cause of an abnormal
PCT is poor timing. Other causes include
cervical stenosis, hypoplastic
endocervical canal, coital dysfunction,
and male factors.
The sample can also be assessed for pH,
mucus cellularity, WBC, and ferning.
◦ Clumping and flagellation of sperm without
Postcoital
progressiontest
antibodies.
(PCT)
are often suggestive of antisperm
Exclusion of Ovulatory Factor
Infertility
To exclude ovulatory dysfunction, the
presence of ovulation must be confirmed.
Also ovarian reserve should be assessed
to exclude oocyte depletion or aging, and
premature ovarian failure.
Confirmation of Ovulation
1. The basal body temperature (BBT)
chart is a simple means of determining
whether ovulation has occurred.
◦ The woman's temperature is taken daily with a
thermometer on awakening, before any
activity, and is recorded on a graph.
◦ After ovulation, rising progesterone levels
increase the basal temperature by
approximately 0.4°F (0.22 °C) through a
hypothalamic thermogenic effect.
◦ As the rise in progesterone may occur
anytime from 2 days before ovulation to 1
day after, the temperature elevation does not
predict the exact moment of ovulation but
offers retrospective confirmation of its
occurrence.
◦ A temperature elevation that persists for less
than 11 days is suggestive but not
diagnostic of a luteal phase defect.
2. Midluteal phase progesterone level
is another test to assess ovulation.
◦ A concentration greater than 3.0 ng/mL in a
blood sample
Exclusion of drawn between
Ovulatory Factordays 19 and 23
is consistent with ovulation, whereas a
Infertility …
concentration greater than 10 ng/mL implies
adequate luteal support.
Exclusion of Ovulatory Factor
Infertility …
3. Daily monitoring of urinary LH has
been widely available given the
proliferation of commercial tests for
home use.
–Using a threshold concentration of 40
mIU/mL, positive testing for urinary LH
has been shown to correlate well with
the surge of serum LH levels that trigger
ovulation.
–Exclusive reliance should not be placed
on urinary LH testing for the detection of
ovulation:
–7% to 8% of women both fertile and
infertile have been shown to have false
positive tests by this means.
Exclusion of Structural Factors
The hysterosalpingogram (HSG)
assesses uterine and fallopian tube contour
and tubal patency and is performed in the
early follicular phase, within 1 week of
cessation of menstrual flow.
This timing minimizes the chances of
interrupting a pregnancy.
Nonsteroidal anti-inflammatory drugs may
be given to prevent cramping.
Prophylactic antibiotics (e.g., doxycycline,
100 mg orally twice daily) are advisable
when the patient has a history of pelvic
inflammatory disease or when
hydrosalpinges are identified during the
study.
Exclusion of Structural Factors

A diagnostic laparoscopy assesses
peritoneal and tubal factors, such as
endometriosis and pelvic adhesions, and can
provide access for simultaneous corrective
surgery.
 Laparoscopy should be scheduled in the
follicular phase and is the final and most
invasive step in the patient's evaluation, unless
the HSG raised suspicion of abnormalities.
 Findings on HSG correlate with laparoscopic
findings 60% to 70% of the time.
 Hysteroscopy may also be included to ensure
that no intrauterine abnormalities were missed
on the HSG.
The Endometrial Biopsy and the
Luteal Phase Defect
An endometrial biopsy evaluates the
response of the endometrium to
progesterone.
The test is usually performed between days
24 and 26 of a 28-day menstrual cycle or 2 to
4 days before anticipated menstruation.
The biopsy documents ovulation by histologic
demonstration of decidualized stroma,
assesses for endometritis, and allows for
histologic dating of the endometrium within 2
to 3 days.
The risks of the procedure are minimal but
include infection, bleeding, interruption of
pregnancy, and uterine perforation.
Treatment
 Before progressing to ARTs, an infertility patient
should undergo treatment for reparable problems
 Anovulation. The WHO stratifies anovulatory
women into three classes:
 WHO Class I: Hypogonadotropic hypogonadal
anovulation encompasses hypothalamic
amenorrhea attributable to low GnRH levels or
pituitary unresponsiveness to hypothalamic
GnRH, with resultant low FSH and serum estradiol
levels.
 WHO Class II: Normogonadotropic
normoestrogenic anovulation involves normal
levels of estradiol and FSH; LH levels, however,
are elevated. This class includes the polycystic
ovarian syndrome (PCOS).
 WHO Class III: Hypergonadotropic
hypoestrogenic anovulation results from
premature ovarian failure or ovarian resistance.
Anovulation
 The vast majority of anovulatory women of reproductive
age fall into WHO class II and, fortunately, this class
proves responsive to ovulation induction.
 The agents most commonly used to stimulate multiple
ovarian follicles are clomiphene citrate (CC), human
menopausal gonadotropins (hMG), and purified
follicle-stimulating hormone (FSH).
 CC, a synthetic, nonsteroidal estrogen agonist-
antagonist, increases the release of gonadotropin-
releasing hormone (GnRH) and subsequent LH and FSH
release.
 CC is useful in women with oligomenorrhea and
amenorrhea, with intact hypothalamic-pituitary-ovarian
axes.
 Women with PCOS often respond to metformin
administered with or in lieu of CC.
 GnRH, hMG, and FSH are used primarily in women
who fail to respond to CC or who have
hypogonadotropic amenorrhea or unexplained
infertility.
Hyperprolactinemia
Bromocriptine is used to induce ovulation
in patients with hyperprolactinemia.
Bromocriptine is a dopamine agonist that
directly inhibits pituitary secretion of
prolactin, which restores normal
gonadotropin release.
The usual starting dose is 2.5 mg at
bedtime to prevent dopaminergic side
effects, which include nausea, diarrhea,
dizziness, and headache.
If Clomiphene Citrate is added if ovulation
does not occur within 3 months after
beginning treatment.
Treatment …
Thyroid problems should be treated
appropriately because both hypothyroidism
and hyperthyroidism may lead to infertility.
Hypothalamic-pituitary axis problems,
problems
including extreme weight gain or loss,
excessive exercise, and emotional stress, can
all impact the secretion of GnRH from the
hypothalamus and cause ovulatory
dysfunction. These must be addressed by
appropriate behavioral or psychological
intervention
Treatment …
Male Factor Infertility:
The evaluation entails examination of the
hypothalamic-pituitary-testicular axis, outflow tract, and
testicular function.
Toxins, viruses, sexually transmitted diseases,
varicoceles, and congenital problems can all influence
infertility.
The initiation of intracytoplasmic sperm injection
(ICSI) has revolutionized treatment of male infertility. As
long as viable sperm can be retrieved by ejaculation,
epididymal aspiration, or testicular biopsy, successful
fertilization and pregnancy can be achieved.
The fertilization rate is 95%, and the pregnancy rate is
comparable to that of in vitro fertilization (IVF
Leukocytospermia
Finding of significant number of leukocytes
(>106/ml) in semen analysis with or without
overt genital tract infection
Chylamydia epididymitis can result in
permanent damage or prolonged
inflammatory response in absence off
persistent organisms.
Empirical treatment with doxycycline or
ciprofloxacin for 4-6 weeks & repeat semen
analysis after 3 months.
Retrograde ejaculation
May occur after prostatectomy, bladder neck
surgery, sympathectomy, DM or multiple
sclerosis.
If ejaculate is absent or no sperm then
diagnosis should be suspected.
Diagnosis is confirmed by finding sperm in a
urine specimen collected after ejaculation>
Sympathomimetics (imipramine 25 mg twice
daily or 50 mg at bedtime, pseudoephedrine
60 mg, or ephedrine 25-50 mg four times
daily, phenylpropanolamine 50-75 mg twice
daily), directed at control of the internal
sphincter
Eugonadotropic
Hypogonadism
Men with severe oligospermia (less than 5
million sperm/mL),
low testosterone levels (less than 300
ng/dL) and an abnormally low
testosterone (ng/dL)/estradiol (pg/mL)
ratio (less than 10)
may benefit from medical treatment with
an aromatase inhibitor.
 Treatment with testolactone 50-100 mg
twice daily or anatrozole 1 mg daily can
normalize ratios and improve semen
quality.
Intrauterine Insemination
 Accepted form of treatment for men with severe
hypospadias, retrograd ejaculation, neurologic
impotence, and sexual dysfunction.
 Artificial insemination has ealso been used as a
means to overcome oligospermia,
asthenospermia, low ejaculate volumes,
antisperm antibodies, and cervical factors.
 HSG is recommended for women over age 35 and
when the medical history or physical examination
raises suspicion of endometriosis or uterine or
tubal infertility factors because IUI is less likely to
succeed in couples with combined male factor
and tubal factor infertility; IVF, with or without
ICSI, is usually a better treatment option
Surgical treatment for male
infertility
Ejaculatory duct obstruction is usually
congenital but can also result from chronic
prostatitis or compression by prostate or
seminal vesical duct cysts and may be
correctable by transurethral resection.
Transurethral resection of an ejaculatory duct
obstruction results in increased semen
volume in approximately two-thirds of
affected men and returns sperm to the
ejaculate in about half of azoospermic.
Surgical treatment for male
infertility
 Varicocele repair is primarily indicated for men with
palpable varicoceles and abnormal semen parameters
having either a partner with normal fertility or treatable
infertility or an interest in future fertility .

Orchiopexy
 Cryptorchidism is associated with a high incidence of
infertility even when it is unilateral; when both testes
are undescended, azoospermia is all but certain.
 if the contralateral testis is normal, fertility may be
preserved.
 Even in adult men with bilateral cryptorchidism,
orchiopexy can result in spermatogenesis and fertility;
at the least, it preserves testicular hormone production.
Vibratory Stimulation and
Electroejaculation
Men with neurologic conditions affecting
the sympathetic system frequently have
dysfunctional or absent emission.
This includes men with spinal cord injuries,
demyelinating neuropathies, diabetes, and
those who have had retroperitoneal lymph
node dissections.
Ejaculation can be achieved with vibratory
stimulation, and in those who don't respond,
electroejaculation can be used to obtain
motile sperm for IUI or IVF and ICSI.
Uterine factors
Such as submucous leiomyomas, intrauterine
synechia (Asherman's syndrome), and
uterine deformities or septa, cause
approximately 2% of infertility.
The mainstay of treatment for these
conditions is surgical correction, usually via a
hysteroscopic approach
Integrity of the cavity should be maintained
by using indwelling intrauterine contraceptive
device for at least 2 months to allow
resumption of regular menstrual shedding.
Infections
Infections of the female and male genital
tracts have been implicated as causes of
infertility.
Chlamydia infection and gonorrhea are the
major pathogens and should be treated
appropriately.
Ureaplasma urealyticum and Mycoplasma
hominis have also been implicated, and, if
positively identified by culture, they should
be treated with oral doxycycline, 100 mg
twice daily for 7 days.
This has been shown to increase the
pregnancy rate in patients with primary
infertility.
Tubal factor
 Tubal factor infertility has become more
prevalent with the increased incidence of
salpingitis.
 Proximal tubal obstruction is identified on HSG.
 Tubal spasm may mimic proximal obstruction,
however, and obstruction should be confirmed by
laparoscopy.
 Treatment consists of tubal cannulation,
microsurgical tubocornual reanastomosis, or IVF.
 Distal tubal disease or distortion can be seen on
HSG and laparoscopy.
 The success of corrective surgery
(neosalpingostomy) depends on the extent of
disease.
ASSISTED REPRODUCTIVE
TECHNOLOGIES
 Since the first successful IVF pregnancy,
delivered in 1978, several techniques have
been developed that enhance our ability to
overcome infertility.
 Among them are the capabilities for embryo
cryopreservation and ovum donation.
 Of all ART procedures nationwide using fresh
nondonor eggs or embryos, 34.3% resulted in
pregnancy according to the 2002 National
Fertility Clinic data, with a total live birth rate
of 28.3%.
 Over 53% of pregnancies resulted in single live
births, whereas 29.4% resulted in twins and
6.8% in triplets or higher multiples.
Miscarriages occurred in 15%, ectopic
pregnancies in 0.7%, and stillbirths in 0.5%
Gamete intrafallopian transfer
 In GIFT, extraction of oocytes is followed by the
transfer of gametes (sperm and oocyte) into a
normal fallopian tube by laparoscopy.
 GIFT requires general anesthesia and does not
allow for visual confirmation of fertilization.
 If pregnancy does not occur, no procedure is
available to determine whether the cause is
failure of fertilization or failure of implantation.
 GIFT contributed to only 0.2% of the ART cycles
performed in 2002. Its diminishing appeal can be
explained by its live birth/retrieval rate of only
25.4% versus 34.0% for IVF without ICSI and the
need for laparoscopy.
Zygote intrafallopian transfer
ZIFT refers to the placement of embryos
into the fallopian tube via laparoscopy
after oocyte retrieval and fertilization.
It combines features of in vitro fertilization
and GIFT.
Similarly, ZIFT's live birth/retrieval rate of
only 26.3% helps explain its diminishing
appeal versus IVF.
ZIFT contributed to 0.5% of ART cycles in
2002
In vitro fertilization (IVF)
 It refers to controlled ovarian hyperstimulation,
ultrasonographically guided aspiration of oocytes,
laboratory fertilization with prepared sperm, embryo
culture, and transcervical transfer of the resulting
embryos into the uterus.
 Although most IVF procedures use fresh oocytes from
the patient, transfer of frozen oocytes and transfer of
donor eggs are also options.
 The overall 2002 live birth/retrieval rate for IVF was
34%.
 For patients undergoing IVF, the pregnancy success
rate varies little by cause of infertility, with a success
rate approximating the overall national rate in
women with most diagnoses except for diminished
ovarian reserve.
Intracytoplasmic sperm injection
In ICSI, a single spermatozoon is injected
microscopically into each oocyte, and the
resulting embryos are transferred
transcervically into the uterus.
The advent of ICSI has revolutionized
fertility treatment for couples confronting
male factor infertility refractory to IUI or
IVF.
The 2002 data demonstrate that the
success rates of ICSI for male factor
infertility compare favorably to routine IVF
without ICSI performed for nonmale factor
infertility (live birth/retrieval rate of 31.9%
versus 34%).
Controlled Ovarian Hyperstimulation (COH)
and Protocols for In Vitro Fertilization
The agents most commonly used to stimulate
multiple ovarian follicles are CC, human
menopausal gonadotropins (hMG), and
purified FSH.
The particular products and protocols used
may be tailored as the treatment proceeds to
boost the chances of an adequate response
and increase the pregnancy rate.
IUI
IVF
Other treatment options

Adoption
Prognostic factors

The main factors influencing the


prognosis in infertility are:
1.couple’s age (especially the
female’s)
2.Cause
3.duration
4.primary or secondary
Thank you…!

66

You might also like