KRIPTORKISMUS

Sit Dolor Amet

DEFENITION
 Cryptorchidism comes from the word cryptos (Greek):
which means hidden and orchis (latin) which means testis.
 The point is a congenital abnormality where after 1 year of age, 1 or 2 testes are not
in the scrotal sac but are still in one place along the normal testicular descent.

EPIDEMIOLOGY
 Incidence: premature babies (21%),  Cryptorchidism incidence rate:
term infants (4.3%) • Neonates <2500 g: 30.3%
 Age 1 year: 0.75-0.8% who remain
• Neonates> 2500 g: 3.4%
cryptorchid
• 12 months old: 1.8%
 70-75%: unilateral cryptorchidism,
the rest are bilateral • > 12 months: 0.8%
• Adult: 0.8%
ETIOLOGY
 The exact cause of cryptorchidism is unclear. Some related things are:
1. Testicular gubernaculum abnormalities
Decline in the testes is guided by the gubernaculum. A large gubernaculum mass will dilate the
testicle, contraction, involution, and traction and fixation of the scrotum will place the testis in the
scrotal bag. When the thesis has been in the gubernaculum scrotum pouch will be absorbed
(Backhouse, 1966) If this structure is not formed or formed abnormally it will cause testicular
maldesensus.
2. Testicular intrinsic defects : Maldesensus can be caused by gonadal dysgenesis where this
abnormality makes the testes insensitive to the gonadotropin hormone.
3. Deficiency of hormonal / endocrine stimulation
• Inadequate maternal gonadotropin hormone causes incomplete decensus. This clarifies the case of
bilateral cryptorchidism in preterm infants when the development of maternal gonadotropin remains in
low levels until the last 2 weeks of pregnancy.
• High cryptorchidism in preterm is thought to occur due to inadequate HCG stimulation of fetal
testosterone release due to immature Leydig cells and immature hypothalamic-pituitary-testicular axis.
• The defect of the hypothalamic-pituitary-gonadal axis will affect testicular descent. The main hormones
that regulate the testes are LH and FSH which are reproduced by basophilic cells in the anterior pituitary
which are regulated by LHRH. FSH will affect the Sertoli cells, seminiferous tubular epithelium. FSH
levels rise in testicular abnormalities.
4. Genetic / hereditary : malformation syndrome, chromosomal abnormalities
RISK FACTOR

Because the exact cause of cryptorchidism is unclear, we can only detect risk factors,
including:
 LBW (less 2500 mg)
 Mothers who are exposed to estrogen during the first trimester
 Double births (twins 2, twins 3)
 Premature birth (gestational age less than 37 weeks)
 Fetal underweight
 Have a father or sibling with a history of UDT
EMBRIOLOGY
 Male genital tract: originates from  End of week 7: intracoelomic testes
urogenital ledge.
Month 3:
 Medial section: form the genital ledge internal desensus testicles are
located above the pelvis
 Weeks 4-5: primitive gonads form Months 8-9:
 Week 6: gonad differentiation external desensus testicles
descend to the scrotum
1. cortical persistence: forming an
ovary  Internal structure of the testes:
2. medullary development: forming
develops in the 3rd month
 External genitalia: arises at week 6
the testes
 called genital tubercles (genital
tubercles)
 shape the penis in men and the clitoris
on woman
Determined by the Y chromosome or X-
Y interaction
EMBRIOLOGY
 Testicular desensus to the scrotum last 3
months intrauterine, mostly completed at
birth
 There are 3 factors that play a role in the  When the position of the testes is relatively
decline process testicles:
1. Anti Mullerian hormone (AMH)
2. Intra-abdominal pressure
3. Androgen hormone factors
THE SECOND AND THIRD STAGES OF THE INFLUENCE
OF ANDROGENS AND GONADOTROPINS
 The process of migration / descent of the
testes involves 3 stages:
1.Nephric displacement
changed, as a result rising mesonephros. At
this stage endocrine factors no role. This
phase is completed in 7 weeks.
2.Transabdominal migration
 Caused by the growth of the gubernaculum
extraabdominal. In this phase Mullerian
Inhibiting substance has a role.
 This phase occurs between weeks 7 and 12
3.Transinguinal migration
 Occurs since the 7th month - birth
EMBRIOLOGY
 CLASSIFICATION

Cryptorchidism can be classified based on etiopathogenesis and location.

1. Based on Etiopathogenesis
 Mechanical / anatomic: attachment, inguinal canal abnormalities
 Endocrine / hormonal: hypothalamic-pituitary-testicular axis disorder
 Dysgenesis: multiple intersex abnormalities
 Hereditary / genetic
2. Based on location:
 High scrotal (supraskrotal): 40%
 Intracaniduli (inguinal): 20%
 Intraabdominal (abdomen): 10%
 Obstruction: 30%
 DIAGNOSIS
1. History
 Generally begins with the parent takes the
child to the doctor with complaints of a small
child scrotum. And if accompanied by
inguinal hernia will be found swelling or
recurring pain in the scrotum.
2. Physical Examination
a) Determination of testicular location
Some positions of the child when examined: supine,
squatting, sitting. Testicular examination must be done
with warm hands. In a sitting position with legs folded or
relaxed in a sleeping position. Then the testes are
touched from the inguinal toward the scrotum by milking.
b) Determination of whether the testicles are palpabel

 History taken: 1. If the testis is palpable some possibilities include: (1)

retractile testis (2) UDT (3) ectopic testis (4).
Ascending Syndrome Syndrome. Ascending
 Have the testes been examined, touched Syndrome testis is a testicle in the scrotum / retractil,
before in the scrotum. but it becomes higher because of the short funicular
spermatikus. Usually only known at the age of 8-10
years. If the testes are palpable, then determine the
 The presence or absence of other position, size, and consistency. Compare with the
congenital abnormalities, such as contralateral testes.
hypospadias, interseks, prunne belly 2. If the testis is impalpable, the possibilities are: (1)
intracanalicular, (2) intraabdominal, (3) testicular
syndrome, and other endocrine disorders atrophy, (4) Agenesis. Impalpable testes are usually
accompanied by inguinal hernias. Bilateral impalpable
 The presence or absence of a family history testes are often associated with other anomalies such
as intersexual, prone belly syndrome.
of UDT
3. Supporting Examination
 Ultrasonography (USG) : Is the first modality in upholding cryptorchidism.
Ultrasound is only effective for detecting testes in the inguinal canal to the
superficial, and cannot detect testes in the intraabdominal
 CT scan : Is the second modality after USG. CT scan can detect intraabdominal
testes. CT scan accuracy is as good as ultrasound on the inguinal testes. False
positives / negatives are usually due to enlargement of the lymph nodes. Can be
distinguished from the testes because of the fat around the lymph nodes.
 MRI : can detect malignant degeneration in cryptorchidism. The disadvantage of
intestinal loops and lymphonodi can resemble cryptorchidism.
 Angiography : accurate but invasive so it is not preferred. Gadolium venography
with MRI is more accurate than a single MRI.
GOVERNANCE

 Non Surgical Therapy : In the form of hormonal therapy. It is recommended before

children aged 2 years, should be 10-24 months. In FKUI therapy after the age of 9
months because almost no more spontaneous decline can occur. Hormones given:
1. HCG : This hormone will stimulate Leydig cells to produce testosterone. Dosage:
Other experts give 3300 IU, 3 times daily for unilateral UDT and 500 IU 20 times 3
times a week. HCH injection should not be given every day to prevent the
desensitization of Leydig cells to HCG which will cause steroidogenic
refractoriness.
2. LHRH : Dose 3 x 400 intranasal ug, for 4 weeks. Will reduce the testicles
completely by 30-64%.
3. HCG LHRH combination - Dosage: LHRH 3 x 400 ug, intranasal, 4 weeks.
Continued intramuscular HCG 5 times daily intervals. Age less than 2 years: 5 x
250 ug, 3-5 years: 5 x 500 ug, over 5 years: 5 x 1000 ug.
 Therapeutic response: decreased testes 86.4%, with follow-up 2 years later the
survival survived 70.6%.
GOVERNANCE

 Surgical Therapy : the goal of surgery is to mobilize the testes, adequacy of the
spermatic vasa supply, adequate testicular fixation to the scrotum, and the
accompanying surgical abnormalities such as hernias.
 Operation techniques on UDT:
I. Orchydopexy Standard
The principle of orchidopexy includes 3 stages
a. Funiculolysis
b. Transfer of the testes into the scrotum (transposition)
c. Fixation of the testes in the scrotum
II. Stephen Flower Orchidopexy
III. Orchydopexy gradually
 COMPLICATIONS

Preoperative
 Inguinal hernias : About 90% of UDT sufferers have ipsilateral lateral inguinal
hernias caused by failure of the closure of the processus vaginalis.
 Torsion Testicles : The incidence of torsion increases in UDT, presumably
influenced by the dimensions of the testes which increase according to the volume
of the testes.
 Testicular trauma : Testicles located in the superficial pubic tubercle are often
affected by trauma.
 Malignancy : The incidence of testicular tumors in the normal population is 1:
100,000, and in UDT 1: 2550.
PROGNOSIS
 According to Docimo, the success of the UDT operation was 92% distal to the
internal inguinal annulus, inguinal location (89%), orchidopexy microvascular
techniques (84%), standard abdominal orchidopexy (81%) staged Fowler-Stephens
orchidopexy (77%), Fowler-Stephens standard orchidopexy (67%).
 UDT usually drops spontaneously without intervention in the first year of life. The
risk of malignancy is higher than normal testes. Fertility in bilateral UDT: 50% have
children, while UDT is unilateral 80%.