August 04, 2016 OBSTETRICS & GYNECOLOGY

*When there is an adequate uterine contraction, the cervix will dilate

ABNORMAL LABOR-DYSTOCIA and effaced.
*Effacement – thinning of the cervix
Dr. Jordias
2. Fetopelvic Disproportion
Dystocia – difficulty in labor  Excessive fetal size – macrosomia from a gestational
Characteristics: diabetic mellitus
 Abnormally slow labor  Inadequate pelvic capacity – anatomical structure of
 Interfere with the orderly progression to spontaneous the bony pelvis
delivery  Malpresentation or position of the fetus – breech,
Abnormalities: transverse lie, compound position
Expulsion forces – Uterus is not contracting properly *Posterior fontanel – dictates the position of the fetal
Presentation, position or development of the fetus head is as it enters the pelvis.
Maternal bony pelvis - 3. Ruptures membranes without labor
Soft tissue of the reproductive tract – minor cause
Labor - adequate uterine contraction of sufficiency, frequency,
Essential Factors of labor (The 3 P’s) intensity and duration to bring about cervical thinning or
Power - related to uterine contraction effacement and dilatation of the cervix.
Passenger – fetus
Passage Starts:
*If there are any abnormalities in the 3 P’s the baby will be delivered via 1. Regular uterine contractions
abdominal route or caesarean delivery  Ask how often the contraction
A. Power Usually ask in a pregnant woman who is in 3rd
Expulsion forces trimester of pregnancy
Uterine contractions  Intensity – mild, moderate or strong
Abdominal pressure  Interval or duration
Voluntary maternal muscles effort *In order to have adequate cervical dilatation or effacement, the interval
B. Passage should be at least 1 or 2 minutes, duration 50 -60 secs, strong uterine
Maternal bony pelvis contraction
Soft tissue of the reproductive tract
C. Passenger: (Fetal Abnormalities) 2. Painful uterine contractions accompanied by:
Presentation a.) ruptured membranes
Position b.) bloody show
Development of the fetus c.) cervical effacement
3. Cervical dilatation: >/= 3--‐4 cm or greater
Common Clinical findings in women with ineffective labor: Assess thru Internal Examination
1. Inadequate cervical dilatation or fetal decent Friedman’s Curve
 Protracted labor (slow progress) – implies on active
phase of labor
 Arrested labor (no progress) – the patient is not really
in labor or inadequate expulsive effort, ineffective
pushing; seen in pelvic division of labor
*Pelvic division of labor – where the cardinal movements
(Engagement – Expulsion) was seen (8cm).
 Inadequate expulsive effort (ineffective pushing)
Review:
*Fundus or upper segment – origin of uterine contraction; active portion
* Cervix or lower uterine portion –passive portion, receives contraction Review:
from the upper segment of the uterus *Latent phase- the patient was not in true labor (< 4cm)
*Active phase – 4 cm dilatation

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3 Phases of Active phase: Review:
1. Acceleration phase *Engagement - Biparietal diameter of the fetal head is at the level of
2. Phase of maximum slope – most important ischial spine or passes the pelvic inlet
3. Deceleration phase – delayed on cervical dilatation; pelvic - When the most dependent portion of the fetal head is in the ischial
division begins (8cm) spine.
*First stage – starts from regular uterine contraction and ends in full - Station: -1, -2, -3, -4 = Floating
cervical dilatation (10cm); dysfunction of labor was usually seen in this - Station: 0 = engaged
stage - Station: +1, +2, +3, +4 = Crowning
*Second stage - starts when the cervix is fully dilated and ends when *Suboccipitobregmatic - shortest diameter of the fetal head (10cm)
from the expulsion of fetus. Phases of Cervical Dilatation: Latent phase of labor (1-2cm)
*Third stage – starts from the fetus expulsion and ends to the delivery
of the placenta Contractions
*Fourth stage- 1-2 hours after the delivery of the placenta
- Mother perceives regular contraction, mild, short
Functional Division of Labor: duration, variable frequency cervical softening and
effacement
Mean duration: 8.6 hours
Prolonged Latent Phase:
 Nulliparas: >20 hours
 Multiparas: >14 hours
Factors that affects duration:
- Sedation, excessive
- Anesthesia, conduction
- Poor cervical condition
- False Labor
Management
- Rest  False labor is common
1. Preparatory Phase – prepares the cervix for labor - Augmentation or Induction labor: OXYTOCIN
Little cervical dilatation (1-2cm dilated) - Cesarean delivery for urgent problem
Changes in connective tissue component of Active phase of Labor
cervix  Rapid rates of cervical dilatation
Sensitive to sedation and conduction  Begins when cervix is 3-4cm dilated
anesthesia Mean duration: 4.9 hours (5 hours)
Average rate of cervical dilatation:
2. Dilatational Phase (active phase – 4cm dilated)
 Nulliparas: 1.2 cm/ hour
Dilatation occurs at a most rapid rate
 Multiparas: 1.5cm/ hour
Unaffected by sedation and conduction  Fetal Descent – Starts at about 7-8 cm dilation, pelvic
anesthesia division
*Give spinal or continues lumbar epidural anesthesia - painless *Primigravida – Effacement before dilatation (1cm dilated cervix but
labor the thinning is already 50 -80% effaced)
3. Pelvic Division (8cm dilated) *Multigravida – Dilatation before Effacement
Begins with deceleration phase
Mechanism of labor occur:
a. Engagement
b. Flexion
c. Descent
d. Internal Rotation
e. Extension
f. External Rotation
g. Expulsion

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PROTRACTION DISORDERS Second stage of Labor: 10cm
- Slower than normal progress of cervical dilatation - Full cervical dilatation up to fetal expulsion
- Less than 1cm/ hr cervical dilatation for a minimum of 4 Mean duration: Nulliparas: 50 mins
hours Multiparas: 20 mins
Protracted active phase dilatation – active phase of labor
- The cervix dilated 4- 6 cm over 3 -4 hours Prolonged Second Stage of Labor:
- Normally the expected dilatation over this period of time Nulliparas:
would be from 4 cm dilated to 7-8 cm cervical dilatation  > 2 hours (without anesthesia)
- This rate of dilatation is slow, even in a first time  > 3hours (without anesthesia)
pregnancy Multiparas:
Treatment:  > 1 hour ( without anesthesia)
 Expectant  > 2 hours (with regional anesthesia)
 Augmentations of labor Factors:
o rupture BOW “stripping”  Contracted pelvic
o Uterotonins (oxytocin)  Large fetus
Protracted Descent – Active phase of labor: 2nd stage of labor:  Conduction anesthesia
Descent  beginning of pelvic division (7- 8 cm dilated)
 Intense sedation
Multiparas - <2 cm / hr
 Persistent occiput posterior -
Nulliparas <1cm/ hr
*posterior fontanel  goes to right  posterior transverse
Adverse Effects:
ARREST DISORDERS:
 Postpartum hemorrhage
- Complete cessation of progress
- No dilatation for 2 hours or more  Infection
Prolonged Deceleration Phase  Infant mortality
Multiparas – > 1 hour
Nulliparas – > 3- 4 hours 3 important cause mortality of the mother:
Secondary Arrest – involve cervical dilatation > 2 hours 1. Hemorrhages
Arrest of Descent – there is an initial descent from 0 to +1 but 2. Hypertension
after that there is no further descent; no progress afterwards 3. Infection
1 hour – nulliparas *8% - obstructed labor
1hour - multiparas
Failure of Descent – no descent at all Normal Uterine Pressure
15 mmHg MVU
Arrest Dilation o The lower limit of contraction pressure
- The cervix is found to be 6 cm dilated on 2 required to dilate the cervix.
examinations, 1 or 2 hours apart 60 mmHg MVU
- No cervical dilation has occurred during the period of o The pressure of normal spontaneous
observation contraction
- Arrest of dilatation is a diagnosis made in the active “Pushing” or “bearing down”
phase of the 1st stage of labor (dilatation of labor) o Propulsion and expulsion o the fetus is brought
by:
First stage of Labor:  Coordinated uterine contractions
Criteria for diagnosis of Arrest  Voluntarily or involuntarily action of
- Latent phase has been completed, with cervix dilated the abdominal musculature during the
4cm or more second stage.
- Uterine contraction pattern of >/= 200 Montevideo Heavy sedation or regional analgesia may reduce the
units(MVU) has been present for 2 hours without reflex urge to push and may impair the ability to
cervical change contract abdominal muscles sufficiently.
Fetal station at onset of Active labor
Engagement - decent of fetal biparietal diameter
 Station 0
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Uterine Dysfunction  Lower incidence of
 Significant advances in its treatment  Non reassuring fetal heart rate patterns
- Prolongation of labor may contribute to perinatal  Operative vaginal delivery
morbidity and mortality  Increased rate of blood loss >500ml
- Use of dilute IV infusion of oxytocin in the treatment  Prolonged sitting or squatting during the 2nd
of uterine dysfunction stage
- Performed caesarean delivery rather than difficult  May cause fibular nerve neuropathy
midforceps delivery when oxytocin fails or  Immersion in Water (birthing tub/ pool)
inappropriate used. o Means of relaxation: contribute to more efficient labor
o No change the rate of cervical dilation, length of labor,
Types of Uterine Dysfunction: route of delivery or analgesia use
o Not associated with chorioamnionitis nor endometritis
1. Hypotonic uterine dysfunction o Maternal blood pressure decreased
 More common o Fetal heart rate was unaffected
 No basal hypertonous o Neonatal complications:
 Uterine contractions have a normal gradient  Drowning, hyponatremia, waterborne infection
pattern (synchronous)  Cord rupture, polycythemia
 Pressure during a contraction is insufficient to
dilate the cervix Active Management of Labor O’Driscoll
2. Hypertonic or uncoordinated uterine dysfunction
(200 summation) Admission at 4 cms
 Basal tone is elevated significantly
 Pressure gradient is distorted Rupture membranes Intact membranes
 More forceful contraction of the
uterine mid- segment than the fundus
 Complete asynchrony of the impulse Amniotomy
originating each cornu
Causes of Uterine Dysfunction After 2 hours
 Epidural analgesia
With progress Without progress
 Chorioamionitis
 Birthing position in 2nd stage labor
Oxytocin infusion
 Water immersion 10 units in 1L D5W
Delivery
Uterine Dysfunction: Reported Cases Oxytocin Stimulation of Labor
 Epidural anesthesia  Criteria
o Can slow labor o Active labor has started
 Lengthening the 1st and 2nd stage of labor o No CPD
 Slowing of the rate of the fetal descent o Ruptured membranes
 Chorioamnionitis o Cephalic presentation
Nowadays, it is called Intraamniotic Infection - o Parity < 6
histopathologic diagnosis o No previous uterine scar
o Uterine infection is a consequence of dysfunction and o Clear amniotic fluid
prolonged labor o No fetal distress
 Birthing Position (Upright position: “birthing chair, Suspect CPD
kneeling, squatting, resting with the back at a 30degree - Diagonal conjugate is short 10cm - normal
elevation) - Pelvic side walls are convergent
o Main benefits:
 4 minute shorter interval to delivery - Ischial spine are prominent
 Less maternal pain - Flat sacrum  Normal: Curve Sacrum
 Enhanced maternal satisfaction (squat) - Narrow subpubic angle

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- Negative Muller – Hillis Maneuver Passage Abnormalities:
*Obstetrical Conjugate – shortest distance from the pubic bone to the
sacral promontory (<1.5cm)
* Diagonal Conjugate – 1.5 – 2 cm
* Pelvimetry – only measures anterior posterior diameter of pelvic inlet
- cannot measure transverse diameter because it is not
accessible.

Precaution
o Monitor fetal heart rate
o Observe uterine contractions – discontinue oxytocin if
>5 contractions in 10 minute period
o Mother never left unattended
o Dose: 10 units in 1000ml of lactated Ringer’s solution GYNECOID - most favorable shape of pelvis for vaginal birth
 IV BOLUS IS NOT GIVEN!!!  Oval shaped
o Wider from side to side than from front to back
Amniotomy  Parallel sides
 If amniotic fluid move out of the cavity leading the fetus to  Dull ischial spines
push out of the vaginal canal  Pubic arch is 90° or wider
• Uses  Normal female pelvis: a rounded oval pelvis with well-
a. Induce or augment labor rounded anterior and posterior segments
b. Internal electronic fetal heart rate monitoring
c. Intrauterine assessment of contraction ANDROID
d. Detect meconium  Male-type pelvis
• Precaution  Small inlet that is heart-shape
a. Minimize risk of cord prolapse  Convergent sidewalls
b. Avoid dislodging the fetal head  Prominent ischial spines
 Narrow pubic-arch
Precipitate Labor and Delivery
 Labor that is extremely rapid PLATYPELLOID
 Nulliparas: >5cm/hr  Flattened gynecoid shape
 Multiparas: >10cm/hr  Short anteroposterior diameter
 Expulsion of the fetus in <3hours after onset of uterine  Wide transverse diameter
contractions  Result in a fetus that traverses the pelvis with its head in a
Results from: transverse or sideways position
 Low resistance of the soft parts of the birth canal
 Abnormally strong uterine and abdominal contractions ANTHROPOID
 Absence of painful sensations and thus a lack of
 Longer AP diameter
awareness of vigorous labor
 Shorter transverse diameter
Maternal Effects:
 Uterine rupture
CALDWELL-MOLOY: Classification of Pelvis
 Lacerations of cervix, vagina, vulva or perineum
Base- greatest transverse diameter of the inlet
 Amniotic fluid embolism
Anterior segment - determines the tendency
 Uterine atony
Posterior segment - determines the type of the pelvis
Neonatal effects:
 Fetal hypoxia, intracranial trauma
 Erb-Duchenne palsy
 Infant may fall to the floor if unattended

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INLET
 Clinically examined thru IE and should look at the diagonal
conjugate
o Distal from the lower part of the symphysis pubis to
the promontory of the sacrum—this distance will give
us the obstetrical conjugate and true conjugate
 Boundaries: the brim
True obstetrical conjugate (TOB): More significant (11cm)
Diagonal Conjugate: 1.5cm – 2cm
Oblique: 13cm – not significant
True Conjugate (AP): 11cm
 CONTRACTED INLET
 Shortest anteroposterior (AP) diameter is less
than 10cm (platypelloid)
 AP diameter is measured manually using
diagonal conjugate,approx 1.5cm greater
 Or if greatest transverse diameter is less than
12cm
o Fetal BPD before labor: 9.5- 9.8cm, hence AP
diameter should be greater than 10cm for fetus to
pass thru.
o Plays an important part in the production of abnormal
presentations—cephalic presentation predominate,
but the head floats freely over the pelvic inlet or rests
more laterally in one of the iliac fossae
o In contracted pelvis: face and shoulder
presentations are encountered 3x more frequently
and cord prolapses 4-6x more often.
MIDPELVIS:
 Landmark: ischial spine (IS) – transverse diameter
 Measure the distance bet the 2 IS thru IE
 More common than contracted inlet
 Frequently causes transverse arrest of the fetal head
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 Obstetrical plane: extends from the inferior margin of
symphysis pubis through the IS and touches the sacrum
near the junction of the 4th and 5th vertebrae
 Transverse line theoretically connecting the 2 IS:
o Divides midpelvis into anterior and posterior portions
 Average midpelvis measurements:
 Transverse/interischialspinous:
o 10.5cm
 Anteroposterior—from lower border of symphysis
pubis to the junction of S4-5:
o 11.5cm
 Posterior sagittal—from the midpoint of the
interspinous line to the same point on the sacrum:
o 4.5 - 5cm
 CONTRACTED MIDPELVIS
o When the sum of the interspinous and posterior
sagittal is less than 13.5cm (normal is 15.5cm)
 Prominent ischial spines
 Convergent pelvic sidewalls
 Narrow sacroiliac notch
OUTLET
- Low obstetrical significance
 Roughly likened to 2 triangles:
o Interischial tuberous diameter constitutes the base
of both (> 8cm)
o Sides of anterior triangle: pubic rami; apex:
inferoposterior surface of symphysis pubis
o Posterior triangle: no bony sides, but is limited at its
apex by the: tip of the last sacral vertebrae
 Decrease in the interspinous diameter and narrowing of
anterior triangle forces the fetal head posteriorly
 CONTRACTED OUTLET
o Defined as an interischial tuberous diameter of less
than 8cm
o Occurs concomitantly with midpelvic contraction
o Plays an important part in perineal tears
ESTIMATION OF PELVIC CAPACITY
 Clinical Pelvimetry
 X-ray Pelvimetry
 Computed Tomographic Scan (CT scan)
 Magnetic Resonance Imaging (MRI)
o MRI Pelvimetry advantages:
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1. Lack of ionizing radiation
2. Accurate measurements
3. Complete fetal imaging
4. Potential evaluation of soft tissue dystocia
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- Inc. FSH and woman approaches menopause 
INFERTILITY - Gyne change in oocyte number and competence
o Day 3 FSH >15mIU/ml – reduced pregnancy
Dr. Jordias rate in IVF
Fecundability
Infertility - Defined as 1 year of unprotected intercourse without  Women who stops using oral contraceptive pills in order
pregnancy. to conceive
Classified as: - Half of the couples will conceive in 3 months
o Primary infertility - In which no previous - 3/4th will conceive in 6 months
pregnancies have occurred. - 90% will conceive in 1 year
o Secondary infertility - In which a prior pregnancy, a Causes of Infertility:
prior pregnancy, although not necessarily a live birth 1. Ovulatory disorders (27 %)
has occurred. 2. Male factors (25%)
3. Tubal disorders (22%)
FECUNDABILITY 4. Endometriosis (5%)
 The probability of achieving pregnancy within a single 5. Others (4%)
menstrual cycle 6. Unexplained factors (7%)
 The fecundability of a normal couple has been estimated at
20 – 25% RELATIVE PREVELENCE OF THE ETIOLOGIES
o Normal = about 90% of couples should  MALE FACTOR: 25-40%
conceive after 12 months of unprotected  Both male and Female factor:10%
intercourse.  FEMALE FACTOR: 40-50%
 Unexplained infertility: 10%
FECUNDITY
*Approximate prevalence of the causes of infertility in the female
 Is the probability of achieving a live birth within a single
(%)
cycle about 90% of couples should conceive after 12
 Ovulatory dysfunction : 30 -40%
months of unprotected intercourse.
 Tubal peritoneal factor: 30 -40 %
Percentage of maternal woman with who is infertility by age:  Unexplained infertility: 10 -15%
 Miscellaneous causes: 10 -15%
Age Infertile (%)
20 to 24 7.0 Causes of Infertility:
Absolute
25 to 29 8.9
 Congenital or acquired irreversible loss of functional
30 to 34 14.6 gametes in either partner
35 to 39 21.9  Absence of reproductive structures in either partner
40 to 44 28.7 Counselling
The older the patient the higher the chance of infertility  Adoption
 Use of gametes
EPIDEMIOLOGY  Surrogacy
 Infertility affects about 10% to 15% of reproductive–age
couples in the United States. INITIAL ASSESSMENT
3 fold increase in office visits:  Initial encounter with the infertile couple is the most
 Increase in media coverage of ARTs important one because
 Delayed marriage and postponement of childbearing - It sets the tone for subsequent evaluation and treatment
Infertility is the problem of the couple
AGE AND INFERTILITY Male partner should be present during the first visit
- Age related decline in fertility: attribute tendency to  His history is a key component in the selection of
depletion diagnostic and therapeutic plans

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Physician should obtain a complete medical, surgical and Immature spermatogonia
gynecological history from the woman
 Menstrual cyclicity, pelvic pain, and previous pregnancy Mitotic division
outcomes Spermatocytes
 Hx of PID, intrauterine device use or pelvic surgery
 Intrauterine exposure to diethylstilbestrol Meiosis
 ROS: Galactorrhea, Hirsutism, Changes in weight (Spermatozoa – 23 chromosomes)
 Development defect: Undescended testes Spermatozoa transverse the epididymis in 12 – 21 days as
 Past genital surgery they mature and become progressively more motile
 Infections: Mumps orchitis
PHYSIOLOGY:
 Previous genital trauma: Medications, Hx of
During ejaculation – release from vas deferens along with fluid
occupational exposures
from prostrate, seminal vesicle, and bulbourethral glands
 Family Hx: Infertility, Premature ovarian failure,
*Semen is gelatinous, but liquefaction occurs in 20 -30 minutes
Congenital or developmental defects, Mental
retardation, Coital frequency, Dyspareunia, Sexual
CAPACITATION
dysfunction
 Series of biochemical and electrical events take place
 Hereditary Conditions: Thalassemia, Tay Sachs
within the sperm’s outer surface membrane before
Disease
fertilization
*Assess the emotional impacts of infertility on the couple
 No capacitation: no fertilization
*Thorough physical examination
Particular attention given to:  Happens when the sperm passed the cervical mucus
- Height
- Weight ACROSOME REACTION
- Body habitus  Release of enzyme of the inner acrosomal membrane
- Hair distribution results in the breakdown of the outer plasma membrane
- Thyroid gland and its fusion with the outer acrosomal membrane
- Pelvic Examination CORTICAL REACTION
Diagnostic Evaluation:  As the sperm penetrates the egg, it initiates a
1. Semen Analysis hardening of the zona pelucida, which prevents
2. Documentation of ovulation penetration by additional sperm
3. Documentation of tubal patency
SEMEN ANALYSIS
Male Factor:  Optimal period of abstinence – 2 -3 days
- Cause of infertility in 20% of infertile couples  Obtained by Masturbation and collected in a clean plastic
- Maybe a contributing factor in as many as 30 – 40% of cup
cases  Taken to the lab within 1-2 hrs of collection
 Male fertility peak at 35 y/o  Entire specimen should be collected, the initial fraction
 Male fertility declines sharply after 35 y/o contains the greatest sperm density
 Increased risk of chromosomal abnormalities  Collection should take place in the location where the
 analysis will be performed
Anterior Pituitary  Degree of sperm molility should be determined after
FSH LH liqeufaction that occurs 15-20 minutes after ejaculation.
Leydig Cells  Sperm motility decline 2hrs after ejaculation
Seminiferous tubules
Testosterone NORMAL SEMINAL FLUIDS ANALYSIS (WHO)
Spermatogenesis Volume >2mL
Sperm concentration >20 million/mL
SPERMATOGENESIS Sperm motility >50% progressive
Spermatogonia  mature sperm cells >25% rapidly progressive
- 75 days Morphology >15% normal form

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Wbc >1million/mL  Sertoli-cell-only
Immunobead or mixed <10% coated syndrome
antiglobulin reaction test  Seminiferous tubule or leydig cell
 Hypogonadotropic hypogonadism
Semen Parameters  Ductal obstruction/young syndrome
Parameter Lower Ref Limit  Varicocele
Semen volume (ml) 1.5 (1.4 -1.7)  Exogenous factors
Total sperm number (M/ ejaculate) 39 (33 – 46) Oligozoospermia
Sperm Conc (M/ ml) 15 (12 -16)  Genetic disorders
Total Motility (PR + NP, %) 40 (38 -42)  Endocrinopathies
Progressive Motility (PR%) 32 (31 -34)  Varicocele/anatomic disorder
Vitality (live sperms %) 58 (55-63)  Maturation arrest
Sperm morphology (normal %) 4 (3-4)  Hypospermatogenesis
 Exogenous factor
pH >7.2  Abnormal volume
No ejaculate
 Ductal obstruction
Semen Analysis: Normal Reference Value
 Retrograde ejaculation
Forward Progression >2 (scale 0 -4)
 Ejaculatory failure
Normal Morphology >50%
 Hypogonadism
>30 % normal
Low volume
>14% normal
 Obstruction of ejaculatory ducts
Round cells < 5 million ml High volume
Sperm agglutination < (scale 0 -3)  Absence of seminal vesicles and vas deferens
 Partial retrograde ejaculation
SEMEN ANALYSIS TERMINOLOGY:  Infection
Normozoospermia  Unknown factors
 All semen analysis is normal  Abnormal motility:
Oligoospemia o Immunologic factors
 Reduced sperm number o Infection
o Mild to Moderate: 5-20 million/mL o Defects in sperm structure
o Severe: <5 million/mL o Metabolic or anatomic abnormalities of sperm
Asthenozoospermia o Varicocele
 Reduced sperm motility o Poor liquefaction of semen
Teratoozoospermia  Abnormal viscosity:
 Increase abnormal forms of sperm o Etiology unknown
Oligoasthenoteratozoospermia  Abnormal morphology:
 Sperm variable all subnromal o Varicocele
Azoospermia o Stress
 No sperm in semen o Infection
Aspermia o Exogenous factors
 No ejaculation (anejaculation) o Unknown factors
Leucocytospermia  Extraneous cells
 Increase white cell in semen o Infection or inflammation
Necrozoospermia Shedding of immature sperm
 All sperm are non viable or non motile SEMEN ANALYSIS
o Sperm volume:
CAUSES OF SEMEN ABNORMALITIES:  Normal value: 1.5 – 5mL
 Abnormal count  Maybe abnormal:
Azoospermia: - Low volume: possibility of retrograde
 Klinefelter’s syndrome ejaculation
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- High volume: relatively long periods of
abstinence or inflammation of the accessory
glands
 Absence of fructose or increase pH:
- Ejaculatory tract obstruction
- Seminal vesicle dysfunction
o Sperm concentration/ Density
 Number of sperm per mL in the total ejaculate
 Cut-off: 60M/mL for normal fertility
 Lower limit: 20 million/mL (WHO)
o Sperm motility
 Percentage of progressively motile sperm in
the ejaculate
 Asthenozoospermia: reduction of sperm
motility
 Cut-off: 50% motility as lower limit of normal
 Others; 40% motility as a criterion for defining
asthenospermia
o Sperm morphology
 Teratozoospermia: Abnormality of sperm
morphology
 >30 % normal forms: acceptable
 TYGERBERG CLASSIFACATION
 >14% normal rate
 4-14% normal morphology: good
prognosis for fertilization
 <4% sperm morphology: bad prognosis
o White blood cell
 Lymphocytes
 Presence of prostitis
 Immature germ cell
 WHO:abnormal ejaculation
 >5 million round cells/mL
 >1 million leukocytes/mL
 Presence of immature sperm cells in ejaculate
is secondary to:
 Defect in spermatogenesis
 Poor prognosis to fertility
SPERM FUNCTION TEST
o Sperm penetration assay(PSA)
 Hamster egg penetration test
 Measures the ability of patients sperm to
undergo capacitation, to fuse with and
penetrate oocytes membrane, to undergo
nuclear decondensation
 Report percentage of eggs successfully
penetrated or count the number of penetration/
egg – 2 or more is normal
“God Heals, We Serve”
o Human zona binding Assay
 Hemizona test
 Examine the ability of the sperm to bind to
zona
Specialized Test
 Assess sperm viability
 Fertilization Potential
- Zona free Hamster Oocyte Test
 Presence of Antisperm Antibodies
 Effect of cervical mucus on sperm viability and function
(Post coital Test)
Further Evaluation
Environmental Toxins and Drug Exposure
 Mean sperm concentration and mean volume
 Marijuana, cocaine, steroids, chemotherapeutic agents,
cimetidine, erythromycin, nitrofurans, spironolactone,
sulfasalazine, tetracycline
 Smoking and heavy coffee consumption
Varicocele
- Abnormal dilatation of veins within the spermatic cord
- Nearly always occur on the left side
- Pathophysiology: Rise in testicular temperature or a
reflux of toxic metabolites from left adrenal or left renal
vein
- Testicular volume
- Impaired semen quality
- In serum testosterone level
Anatomic Abnormalities:
Congenital Abnormalities
 Hypospadias or cryptorchidism
 Congenital absence or obstruction of vas deferens or
ejaculatory
Retrograde Ejaculation
 Post – ejaculatory or catheterized urine specimens
 DM, some neurologic conditions, after bladder or
prostatic surgery
Trans by DARIANNE 11
August 04, 2016 OBSTETRICS & GYNECOLOGY
Endocrine Abnormalities - Injection of embolizing agents
 Hyperprolactinemia - Therapeutic benefits: controversial
 Hypogonadotropic Hypogonadism ( LH, FSH, Treatment:
Testosterone) Artificial Insemination
 Hypergonadotropic Hypogonadism ( LH, FSH, - Placement of whole semen or processed sperm into the
Testosterone) female reproductive tract
 Karyotype: 47 XXY - Permits sperm – ovum interaction in the absence of
intercourse
Drugs that impair Male Fertility: - Intravaginal insemination performed in cases severe
1. Impaired spermatogenesis coital dysfunction
a. Sulfasalazine
b. Methotrexate ARTIFICIAL INSEMINATION
c. Nitrofurantoin  Intrauterine Insemination
d. Colchicine - Placement of about 0.3 to 0.5 ml of washed
e. Chemotherapy processed and concentrated sperm into the
2. Ejaculation Failure intrauterine cavity by transcervical
a. Beta blockers catheterization
b. Antidepressants  Intracervical insemination
c. Phenothiazines - Maybe performed either with unwashed or with
3. Erectile Dysfunctions processed specimens
a. Beta blockers ---------------------------------- END  ----------------------------
b. Diuretics
c. Metoclopromide
4. Drugs of Misuse
a. Anabolic Steroids
b. Cannabis
c. Heroin
d. Cocaine
Treatment:
 Treatment of reversible endocrine or infectious causes
of subfertility, such as STD and thyroid disorders, tends
to be efficacious
 Medical therapies for other causes of male factor
infertility are severely limited.
Medical Therapy:
 Clomiphene Citrate – Estrogen agonist and partial
antagonist
- Used to treat male infertility of idiopathic origin
- Acts on the hypothalamic pituitary axis and in
men, increases serum levels of LH, FSH and
testosterone
- Treatment with CC yields little improvement in
semen parameters and no improvement in
pregnancy rates
 GnRH - hypogonadotrophic, hypogonadal males
 Antisperm Antibodies – Condoms, Glucocorticoids
Surgical Therapy:
Varicocele
- Involves interruption of the internal spermatic vein
- Laparoscopy
- Open surgery
Trans by DARIANNE 12
“God Heals, We Serve”