Data that should be recorded:
• General medical history: 1)diabetes may cause ejaculatory dysfunction and retrograde ejaculation; 2) multiple sclerosis, that can also disrupt the ejaculatory reflex; 3) postpubertal mumps that may be followed by testicular atrophy in 36%, among others
• Recent febrile illness that may have interfered with semen production, causing an abnormal semen analysis result
• All previous pregnancies
• Any existing problems with sexual functioning (impotence or ejaculatory disturbances)
• Any genitourinary infection
• Maldescent of one or both testes
• Any surgery (especially in the genital area such as: herniorrhaphy)
• Drug use (certain drugs affect sperm production and sexual behavior: Sulfasalazine and cimetidine may be gonadotoxic. Antihypertensives, antipsychotics, and antidepressants can all cause ejaculatory dysfunction. Anabolic steroids can cause depression in the gonadotropin drive to the testes and a subsequent reduction in spermatogenesis. Vasectomy may lead to the production of antisperm antibodies, which can interfere with sperm function)
• Family history may suggest inherited disorder
Laboratory examination
If laboratory sperm examination, that comprises physical, biochemical and sperm count parameters are normal, there is no necessity for pelvic examination.
If the results of the sperm analysis are abnormal, the physical examination, apart from the urogenital system, should include:
Examination:
• The scrotal contents (examined with the man standing)
• Varicocele
• Size (volume) of the testes (graded with Prader orchidometer)
• Palpation of the epididymis (presence of cysts or nodularity arise as a secondary infection)
• Palpation of the vas deferens (bilateral absence explains a finding of azoospermia, indicating possible presence of cystic fibrosis [CF])
• Inguinal canal should be palpated for hernia or maldescended testicles
• The penis examined for hypospadias or phimosis
Observation of disproportionate limb length and height, gynecomastia, reduced body hair, a “bodybuilder” physique.
Investigations
The criterion for performing a test depends on whetherthe results will be of value during management. Currently, there are no standard universally accepted protocols for investigation of subfertile couples, although guidelines have been published by the World Health Organization (WHO), the Cambridge University Press in 1993, and the Royal College of Obstetricians and Gynaecologists published in London in 1998.
Male
Semen is body fluid, that is viscous in nature, and contains sperms and seminal plasma.
The primary investigation is a semen analysis performed after 2–5 days’ abstinence. If the semen analysis is found to be abnormal, it is important to repeat it.
Sperm parameters according to the WHO criteria:
Normal ejaculate
Volume is between 2 and 6 ml.
Volume distribution:
• 65% is from seminal vesicles
• 30-35% is from the prostate
• 5% from the vas
Liquid distribution:
• Urethral and bulbourethral glands – 0.1-0.2 cc, viscous, clear
• Testes, epididymides, vasa deference - 0.1-0.2 cc,, sperm present
• Prostate – 0.5-1.0 cc, acid, watery
• Seminal vesicles – 1.0-3.0, gelatinous, fructose positive
Normal sperm analysis
Biophysical characteristics:
• Volume: 1ml-6ml
• Liquefaction – within 30-60 minutes
• Color – light gray
• PH – 7.2-8.0
Sperm analysis:
• Concentration: 20 million/ml up to 200 million/ml
• Total number of sperm: >40 million
• Motility: 50% or more
• Rapid progressive motile sperm >25% (velocity > 20 microns/second)
• Rapid + slow progressive motile sperm >50% (velocity 5 and 20 microns/second)
• Nonprogressive: turning in circles in one place or no forward movement
• Immotile spermatozoa: completely nonmotile
• Morphology: 30% or more normal shapes (WHO 3rd edition criteria) or 14% or more (WHO 4th edition, strict or Kruger [published in 1988 in Fertil Steril])
Normal appearance of sperm:
• Head has an oval shape (4-5 micron length)
• Light fore-part (acrosome 40-70%)
• Dark rear-part
• Only one tail – without twisting behind or curving
• Middle part shouldbe a bit thinner (maximum with 1 micron)
• Clumping: minimal
• Presence of white or red blood cells: minimal less than 1/million/ml
• No hyperviscosity (thickening of seminal fluid)
The 1987 WHO Manual Describes a Normal Spermatozoon:
Oval head shape with a regular outline and acrosomal cap covering more than one-third of the head surface
The head: length: 3-5 µm, width: 2-3 µm
The midpiece: 7-8 µm, long, straight and regular in outline, slender, less than one-third of head width
The tail: at least 45 µm in length, slender, uncoiled and regular in outline.
Anatomy of the sperm Different sperm pathology
A camera for sperm count
Biochemical characteristic of the semen analysis:
Epididymal markers
Alpha-glucosidase (neutral) 20 μU or more per ejaculate
Carnitine 0.8-2.9 mmol per ejaculate
Glycerophosphocoline
Prostate markers
Zinc (total) 2.4 mmol or more per ejaculate
Citric acid
Acid phosphatase
Semen analysis
Citric acid (total) 52 mmol(e) or more per ejaculate
Acid phosphatase (total) 200 U or more per ejaculate
Seminal vesicle marker
Fructose (total) 13 mmol(e) or more per ejaculate
Prostaglandins
Definitions of semen pathology
• Oligozoospermia - When sperm concentration is < 20 million/ml
• Asthenozoospermia - Fewer than 50% spermatozoa with forward progression
• Teratozoospermia - Fewer than 50% spermatozoa with normal morphology
Oligoasthenoteratozoospermia (OTA) Signifies disturbance of all the three variables
Necrozoospermia: Nonviable ("dead") sperm
Semen analysis
Polyzoospermia: Excessively high sperm concentration
Hypospermia: Semen volume < 1.5 ml
Hyperspermia: Semen volume > 5.5 ml
Aspermia: No semen volume
Pyospermia: Leukocytes (germ fighter cells) present in semen
Hematospermia: Red blood cells present in semen
Reasons for poor sperm analysis not really related to the sperm itself
Incorrect semen collection technique (sample is not collected properly, or if the container is unclean)
Long time interval between providing the sample and reaching the laboratory
Too short an interval since the previous ejaculation
Recent systemic illness in the last 3 months
Antisperm antibody test of immunoglobulin class A (IgA) and IgG
Causes of antisperm antibodies include: Injury to the testicle, infection, surgical procedures (such as vasectomy).
Indications:
Sperm agglutination
Reduced motility
Interference of sperm binding by the zona pellucida
Tests available include:
Sperm immobilization
Sperm agglutination
Indirect immunofluorescence
Enzyme-linked Immunosorbent assay
Radiolabelled antiglobulin assay
Immunobead Rosette Test: most informative, can identify antibody classes (IgG, IgA, IgM) and location on the sperm cell (head, body or tail)
Causes for Male Infertility
• Chromosomal:
Klinefelter syndrome (47 XXY),
XX male dyndrome
XXY syndrome
Y-chromosome abnormalities
• Testicular:
Undescended testis
Varicocele
Orchitis (inflammation/infection of testis)
Injury
Vasal obstruction
Cystic fibrosis mutation
Radiation/chemotherapy damage to the testis
Drugs that damage testis
• Hormonal:
Disorders of pituitary and testicular hormone activity
• Other organs:
Erectile problems
Ejaculatory problems
Vasectomy
Nerve injuries
Penile abnormalities
Coital problems
• General health:
Liver and kidney disorders, sickle cell disease
• Life-style issues:
Obesity, smoking, diet, exercise and psychological factors
Initial Tests for Immediate Differential Diagnosis:
Hormonal profile for the following impairments:
Oligospermia/azoospermia
Impaired sexual function
Evidence of endocrine disorder
Luteinising hormone (LH)
Follicle-stimulating hormone (FSH)
Testosterone (T)
Prolactin (PRL)
If the hormonal levels and testicular size are normal, then the male is likely to have obstructive azoospermia.
Urine analysis:
Indicate infection
Ultrasound of testis:
Detect varicocele
Hydrocele
Undescended testis
Atrophic testis
Chromosomal analysis for the following impairments:
Oligospermia/ azoospermia
High FSH levels
Azoospermia and small testes
Nonpalpable vas deferens indicates CF gene mutation and needs chromosomal analysis
Testicular biopsy:
Azoospermia to differentiate between obstruction and primary testicular failure
Drugs Linked to Male Infertility by Decreasing Spermatogenesis
Spironolactone (part of many antihypertensive regimens)
Sulfasalazine (treatment of inflammatory bowel disease)
Colchicine (acute and chronic control of gout and suppression of familial Mediterranean fever)
Allopurinol (alters uric acid metabolism)
Anabolic steroids (weight lifters and body building)
Cyclosporin (component of immunosuppressive regimens used in renal and liver transplant recipients)
Chemotherapeutic agents (treatment of malignant or cancerous conditions)
Nonobstructive Azoospermia or Severe Oligospermia
Chromosomal abnormalities:
Y-chromosome microdeletions of the azoospermia factor region (AZF) in Yq11
Karyotypic abnormalities such as sex chromosome aberrations (Klinefelter syndrome) or translocations
Inheritance of CF genes resulting in vasal aplasia (this can appear as congenital bilateral absence of the vas deferens (CBAVD), in which men have no other phenotypic expression of CF).
Testicular biopsy
Diagnostically used for differentiating obstruction and testicular failure.
Today, testicular biopsy has an additional therapeutic role in sperm retrieval for use in intracytoplasmic sperm injection (ICSI).