KELOMPOK 23 D

 OEYI MUTIA SATIFA 1710311001

 NURUL IZZAH 1710311037
 IKHLASIA AMALI MAHZUM 1710311070
 MUHAMMAD IRFAN JAMIL 1710312051
 HASNA SOFIYA BUNTORO 1710312060
 TESSA YOLANDA 1710312075
 NAILATUL FADHILA 1710312083
 RIZKI ANUGRAH 1710312090
 EURENA MAULIDYA PUTRI P 1710313045
 SKENARIO 1 : KENAPA ANDI BERBEDA DENGAN
TEMANNYA ?
Andi, laki-laki umur 7 th merasa malu dengan teman2 lainnya karena selalu BAK
jongkok. Ketika bertanya pada ibunya, ibu juga bingung melihat kondisi Andi. Ibu
membawa Andi ke puskesmas. Dari hasil anamnesis diketahui ibu mempunyai riwayat
penggunaan kontrasepsi hormonal sebelum kehamilan Andi. Dari pemeriksaan dokter di
puskesmas hasil inspeksi terdapat hipospadia, mikropalus, kordae, skrotum bifidum dan
pada palpasi gonad hanya teraba satu di sebelah kiri. Dokter menyimpulkan bahwa Andi
menderita kelainan kongenital dan perlu dirujuk untuk diagnosis dan tatalaksana lanjutan.
Sampai di RSUP kasus Andi di diskusikan oleh sekelompok dokter muda dan
preseptor. Dalam diskusi tersebut preseptor menanyakan kepada mahasiswa bagaimana
proses organogenesis genitalia laki-laki dan perempuan, dan apa yang membedakannya.
Salah satu mahasiswa menjawab karena perbedaan kromosom dan ada peran gen SR-Y.
Dalam diskusi juga dipertanyakan kenapa si Andi mengalami kelainan di atas.
Bagaimana komplikasinya nanti, bagaimana pula kalau gangguan ini terjadi pada
perempuan. Selanjutnya didiskusikan juga tentang investigasi yang harus dilakukan seperti
karyotyping, analisis gen SR-Y, pencitraan radiologi untuk menyingkirkan kemungkinan
kelainan bawaan urogenital lainnya dan untuk mendapatkan diagnosis pasti sehingga bisa
dijelaskan jenis kelamin sebenarnya dan dilakukan penetapan jenis kelamin, yang
kesemuanya akan melibatkan multidisiplin.
Sebagai dokter di layanan primer bagaimana saudara menjelaskan ini semuanya?
 Hypospadias: congenital abnormalities in which the urethral
estuary is located on the ventral surface and is more proximal
than it should be
 Micropalus: a condition where the length of the penis when
not erect is less than 2.5 SD below average, the shape of the
penis is normal but the shaft of the penis is shorter.
 Cordae: curvature of the penis due to congenital anomalies,
especially when erect
 Bifidum scrotal: imperfect closure of the scrotum so that
there is a gap between the two scrotums
 SRY Genes: genetic factors that play a role in the
differentiation of the gonads into the testes
 Karyotyping: a method to see the size, number, shape, and
type of chromosomes.
1. Why does Andi always squat urination?
2. What is the effect of hormonal contraception with
abnormalities experienced by Andi?
3. What is the interpretation of the physical
examination done by the doctor at the puskesmas?
4. What congenital disabilities did Andi suffer from
and what causes it?
5. How is the examination carried out for diagnosis
and what is the follow-up management?
6. What is the process of genital organogenesis of
men and women and what distinguishes it?
7. How are male and female chromosomes
different and what is the role of the SRY gene?
8. What are the complications that arise from
Andi's abnormalities and what if they occur in
women?
9. What are the indications for Karyotyping, SRY
gene analysis, and radiological imaging in
Andi's case?
10. What are other possible urogenital
abnormalities that can occur?
11. What is the procedure for determining the sex?
In squat urination →emptying vesica urunaria is better.
But in boys, squat urination can be suspected of
experiencing hypospadias abnormalities, this is because
in hypospadias abnormalities, when squat urination
urinating will radiate weakly because the external
urethral orifice is in the ventral region.
Hispospadias →occur due to exposure to estrogen /
progesterone during pregnancy.
Use of hormonal contraception before pregnancy→ the
relationship is not clear.

Risk factors for hypospadias:

• Use of hormonal contraception in trimester 1
• High estrogen environment→ use of insecticides and
pesticides
• Exposure to diethylstilbestrol
• The hypospadias : external urethral orifice are in the
ventral part
• Micropalus :penis size smaller than normal size
• Bifidum scrotal : there is a gap in the scrotum that can
cause genitalia ambiguity.
• Kordae : scar tissue that causes the penis to bend
toward the ventral, especially when erect
• The right testis does not descend on the gonad
palpation (unilateral cryptorchidism) : often coincides
with hypospadias
Disorder of Sex Development → risk factor for hypospadias (due
to estrogen exposure).

a. Clinical symptoms: pain during urination and erection

b. Inspection: physical inspection by inspection according to
what has been done in the module.
c. Laboratory tests: not required
d. Radiographic examination: needed to rule out other possible
congenital diseases.
e. Management: uretroplasty
 Organogenesis process →at week 6 gonads in the fetus are still
bipotent On the XY chromosome there is the SRY gene which
triggers gonad differentiation into the testes. Duct wolfii →
develops into the male genitalia
 In the male genitals there are Leydig cells and Sertoli cells,
 Leydig cells produce the hormone testosterone which will induce the
formation of epididymis
 Sertoli cells produce anti-Mullerian hormone which inhibits the
development of the Mullerian duct.
 The differentiator: the SRY gene is only found on the Y
chromosome
 In the case of cryptorchidism, testicles that do not descend into
the scrotal cavity may experience necrosis due to temperature
differences in the abdomen and in the scrotal cavity, this can
cause infertility.

Karyotyping:
• See the size, shape and number of chromosomes
• Analyze chromosomes to find out the real sex
SRY Gene Analysis:
• Analyze whether there is an SRY gene that functions in triggering gonad
differentiation
Radiology:
• In the case of cryptorchidism to see whether undescended testicles are in
the scrotal cavity in the abdomen
Disorder of Sex development (DSD)
• phimosis
• Paraphimosis

By doing karyotyping analysis so that the gender is genetically clear

1. Epidemiology congenital abnormalities in the urogenital
system
2. Etiology and risk factors congenital abnormalities in the
urogenital system
3. Pathogenesis and pathophysiology congenital
abnormalities in the urogenital system
4. Diagnosis congenital abnormalities in the urogenital
system
5. Therapy congenital abnormalities in the urogenital system
6. Complications and prognosis congenital abnormalities in
the urogenital system
 Polycystic kidney disease is a progressive genetic disorder
that attacks the kidneys. Polycystic kidney disease is
characterized by the emergence of a kidney cyst that
enlarges progressively, this disease can also attack the liver,
pancreas, heart, and brain.
 In the US: covering 11% of dialysis and transplant patients
 8-10% are autosomal dominant polycystic kidney disease
 Indonesia: 2.21% of patients with terminal kidney failure
 Around the world
 Prevalence 1-5 / 1000 inhabitants
 Male = female
 The US incidence is 6000 people per year
 Autosomal Resesif Polycystic Kidney/ARPKD
 Autosomal Dominant Polycytstic Kidney/ADPKD
 Caused by mutations in a gene that has not been identified
on chromosome 6p. Serious manifestations are usually
present at birth, and babies die quickly from kidney failure.
The kidney shows many small cysts in the cortex and medulla
so that the kidneys look like a sponge.
 It is sent down recessively, not visible to both parents
 Both parents must have recessive genes
 25% probability
 1 in 2 children may be carriers of the gene
 It is thought to be due to the failure of fusion between the glomerulus
and the tubules resulting in the collection of fluid in the dead-end
channel. The larger cyst will suppress the renal parenchyma so that
ischemia occurs and slowly kidney function will decrease.
Hypertension can occur due to ischemia of kidney tissue which
causes an increase in angiotensin rennin.
 It used to be called adult polycystic kidney disease because
it usually manifests at the age above 30 years. It turns out
later to be found in fetuses, infants and young children so
now it is called PGPDA
 Polycystic kidney disease in adults or autosomal dominant
polycystic kidney disease does not cause symptoms until the fourth
decade, when the kidneys have enlarged enough. The symptoms
caused are
 1. Pain
 2. Hematuria
 3. Urinary Tract Infections
 4. Kidney enlargement
 5. Brain Vascular Aneurysm
Frequency Symptoms (%)
Stomach ache 62
Lumbago 50
Hematuria 35
Headache 27
Gastrointest disorders 15
Nocturia 14
Kidney colic 13
Dysuria 9
Polakisuria 9
Polyuria 8
 Diagnosis by taking anamnesis, physical examination,
supporting examination.
 One or both kidneys are enlarged, bumpy
 Organ abnormalities found outside the kidney: liver
cysts (40-70%), splenic cysts (5%), pancreas (10%),
lungs (5%), thyroid, brain, testes and ovaries.
Cerebral artery aneurysm 10%, colonic diverticulum
32%, cardiac valve abnormalities 18%
 Horse tread kidney was also found, immovable sperm,
corneal dystrophy, nail deformity, etc.
 1. urine examination: proteinuria, hematuria, leukosituria,
sometimes bacteriuria
 2. Blood tests: In diseases that are advanced and show uremia,
and anemia due to chronic hematuria
 3. Renal ultrasound
 4. MRI and CT Scan
 5. Biopsy
 Treatment for autosomal recessive polycystic kidney disease
(ARPKD) and autosomal dominant polycystic kidney disease
(ADPKD) is supportive which includes careful management of
hypertension
 ARPKD and ADPKD which develop into kidney failure are
dialysis and kidney transplantation and in ADPKD treatment
aims to prevent complications and maintain kidney function
such as therapy in controlling hypertension and urinary tract
infections.
 If kidney failure has been found, conservative care is taken in
the form of a low protein diet. If kidney failure is advanced,
dialysis or even kidney transplantation is needed.
Hypertension is controlled with antihypertensive drugs such
as ACEI (such as Katopril, enalapril, lisinopril) or ARB (such
as Telmisartan, losartan, irbesartan, cardesartan)
 Large cysts cause blockages in the pelviokalises or urinary
system. Treated by percutaneous cyst puncture or surgery
 Cyst or perirenal hemorrhage. Causing extreme pain in the
patient. Overcome by analgesics, bed rest and surgery if
necessary.
 Infection, treated with adequate antibiotics such as
complicated pyelonephritis therapy
 Urolithiasis (10-34%)
 Nephrocalcinosis
 Malignancy
 Terminal kidney failure
 Two distinct renal masses lying vertically on either side of the
midline & connected at their respective lower poles by a
parenchymatous or fibous isthmus that cosses the midplane
of the body, forming a “U” shape at the isthmus.
 Most common disorders seen horseshoe kidney are turner
syndrome and trisomy 18
 Occurs in 0.25% of the population, or about 1 in 400 persons
 More common in males, 2:1
 Mechanical fusion
 horseshoe kidney is formed during organogenesis, when the
inferior poles of these early kidneys touch, fusing in the lower
midline. The theory of mechanical fusion is valid for horseshoe
kidneys with a fibrous isthmus.
 Teratogenic event
 abnormal migration of posterior nephrogenic cells, which then
coalesce to form the isthmus.
 Mainly asymptomatic – autopsy finding
 UTI and fever in neonates
 Nausea
 Abdominal discomfort
 Kidney stnes and UTI at greater frequency than those without
renal fusion
 Renal USG
 Blood test
 Urine test
 Voiding cystourethrogram (VCUG)
 Intravenous pyelogram (IVP)
 Kidney stones
 Hydonephrosis
 Wilm’s tumor
 Renal cancer
 Hypospadias is an abnormality of anterior urethral and
penile development. The urethral opening is ectopically
located on the ventral aspect of the penis proximal to the tip
of the glans penis, which, in this condition, is splayed open.
 1 in 300 births of boys.
 The incidence rate is 3.2 out of 1000 live births.
 The most often anomalies.
• Based on the location of the urethral estuary after a cord
connection, Browne (1936) divides into 3 major sections:

Sumber : Dasar-dasar Urologi Basuki Edisi 2

 There is no ventral prepuce so the dorsal prepuce becomes
excessive (dorsal hood).
 Often accompanied by a cord (penis angulation to the
ventral).
 Children and adolescents: there are no significant physical
problems.
 Adult: chordee will inhibit sexual relations.

1. Infertility can occur in penoskrotal or perineal hypospadias.

2. Can arise meatus stenosis that cause troubled when
regulating urine.
3. Cryptorcidismus often occurs.
The purpose of the therapy :
1) Penile cosmetics (reconstruction) to restore micturition and sexual
function to normal. Sexual function: straight erection and strong
ejaculation.
2) The penis can grow normally

Reconstruction stages:
a. Chord correction (orthoplasty)
b. Make neourethra from penile skin (uretroplasty): 6 months after
orthoplasty
c. Make a glans
1. Edema: due to tissue reaction
2.Hematom (collection of blood under the skin): can be
prevented by a bandage for 2-3 days after surgery
3. Uretrocutaneous fistula: the most frequent complications
4.Striktur: located in proximal anastomosis
5. Diverticulum: occurs when neourethral formation is too wide
or there is meatal stenosis which results in further dilatation
6.Residual chordee / recurrent chordee: due to imperfect cord
release which does not make an artificial erection during
surgery or excessive scar formation in the ventral penis though
it is very rare.
Good, with adequate therapy:
a.Delete chordee
b. Restructuring the meatus hole through surgery.
 The prepuce is used for reconstruction, so hypospadias
should not be circumcised.
 Chordee can occur without hypospadias, treated by releasing
fibrosis tissue to improve the function and appearance of the
penis.
Epispadias is a rare type of
congenital malformation of
the penis in which the urethra
ends in an opening on the
upper aspect (dorsal) of the
penis.
 Around 1/120,000 male and 1/500,000 female births
 Penopubic Epispadia has the highest incidency
 Hormonal • The hormone that is refer
here is androgen hormone that
disorder or organogenesis or the absence
imbalance receptor.

• Occurred because of the

Genetics androgen synthesis

• Pollutants and substance

Environment teratogenic that may result in m
 Penopubic epispadias: This is where the urinary meatus is
found close to the body, potentially not on the penis but near
the pubic bone at the base of the penis.
 Penile epispadias: The urinary meatus is found on the shaft of
the penis, anywhere before the head of the penis but above
the base where the shaft meets the body.
 Glanular epispadias: This is where the urinary meatus is
found on the head of the penis, but on the top rather than in
the standard location at the tip.
Urethral opening
Difficulty with
is located at the
targeting while
dorsal part of the
urinating
penis

Chordae Incontinensia
 History collection
 Physical examination
 urine tests,
 imaging studies including ultrasound or CT scans, X- rays
The main treatment for isolated epispadias is a comprehensive
surgical repair of the genito-urinary area usually during the
first 7 years of life, including reconstruction of the urethra,
closure of the penile shaft and mobilisation of the corpora.
 The Modified Cantwell Ransley Repair: The modified
Cantwell technique involves "rebuilding" the penis. It takes
some of the penis apart to move the urethra to a more normal
position. The Mitchell Technique
 The Mitchell technique involves taking the penis apart
completely, then putting it back together. This is done so the
urethra is in the most functional and normal position, and
dorsal bend (chordee) is corrected.
 Recurrence
 Sexual problems
 Incontinence
 UTI
 Infertility
 Psycho-social stress
Twisting of spermatic cord leading to decreased of blood flow
to the testicle resulting in ischemia, infarction, and tissue
necrosis
 Most common cause of acute scrotal pain in prepubertal boys
 Torsion present in 3.2% of all children presenting to the ED
with scrotal pain

Risk factor:
 History of cryptorchidism
 Horizontal testicular lie
 Increased spermatic cord length
 The etiologic factors involved in intravaginal testicular
torsion include congenital anomaly, bell clapper deformity,
undescendes testicle, sexual arousal or activity, exercise,
active cremasteric reflex, cold weather
 Contraction of the spermatic muscles shortens the spermatic
cord and may initiat testicular torsion
 Torsion may occur in either
- Clockwise or
- Counterclockwise direction
There are 2 types of testicular torsion:
1. Intravaginal Torsion
 Intravaginal torsion is the more
common type, occurring most
frequently at puberty
 It results of anomalous suspension
of the testis by a long stalk of
spermatic cord, resulting in
complete investment of testis and
epididymis by the tunica vaginalis
 This anomaly has been likened to a
bell-clapper
2. Extravaginal Torsion
 Most often occurs in newborns without the “bell-clapper”
deformity
 It is thought to result from a poor or absent attachment of the testis
to the scrotal wall, allowing rotation of the testis,epididymis, and
tunica vaginalis as a unit and causing torsion of the cord at the
level of the external ring
 Torsion occurs as the testicle rotates between 90° and 180°,
compromising blood fow to and from the testicle
 Complete torsion usually occurs when the testicle twists 360°
or more; incomplete or partial torsion occurs with lesser
degrees of rotation. The degree of torsion may extend to 720°
 Testicular salvage is most likely if the duration of torsion is
less than 6-8 hours. If 24 hours or more elapse, testicular
necrosis develops in most patient
 Sudden onset of scrotal pain (less frequently, abdominal or
inguinal pain)
 Nausea and vomiting
 History of blunt trauma ( 10% of patients)
 History of similar pain in the past
 Unilateral tender, firm testicle
 Scrotal erythema, edema and swelling
 Affected testicle typically higher than the unaffected one
 Loss of cremasteric reflex
30% of males with normal testicles will have an absent
cremasteric reflex
 Stimulation of the skin on the front and inner thigh ( over
Scarpa’s triangle) retracts the testis on the same side. Stimulus
usually causes cremasteric muscle contraction
 Normal: Cremasteric reflex present (testicle rises). Seen in
epididymitis
 Abnormal: cremasteric reflex absent ( no testicle rise). Suggest
testicular torsion
 The diagnosis of testicular torsion should be pursued in any
patient with acute scrotal pain
 Physical exam, clinical features and imaging all have
significant limitations
 In patients with a high suspicion for torsion, emergent
surgical consultation should not be delayed by diagnostic
 All patients with suspicion for testicular torsion should have immediate
consultation with a urologist for potential operative exploration and repair
 Establish IV access and provide analgesia

 Manual detorsion

- Can be attempted if urology consultation is not immediately available

- May be successful in 25-80% of testicular torsion cases

- Procedure

 Place patient supine

 Provider stands at the patient’s feet

 Apply “open book’ rotation: rotate affected testicle away from midline

 Rotation required may be anywhere from 180°-720°

 a condition in which the foreskin of the penis cannot
be pulled back past the glans. A balloon-like swelling under
the foreskin may occur with urination. In teenagers and
adults, it may result in pain during an erection, but is
otherwise not painful.Those affected are at greater risk of
inflammation of the glans, known as balanitis, and other
complications.
 Congenital phimosis (physiology phimosis, false phimosis)
 Aquired phimosis (pathologic phimosis, true phimosis)
 Physiological phimosis is the result of adhesion of the
epithelial layers between the inner prepuce and the glans
penis. Penile erections that occur periodically make the
prepuce dilated slowly so that the prepuce becomes retractile
and cannot be stretched proximal. So as we get older
physiological phimosis will disappear.
 Poor hygiene in the area around the penis and the
presence of recurrent balanitis or balanophostitis leading to
scar formation in the prepuce orificium can result in
pathological phimosis.

Forced retraction of the prepuce can also result in

small injuries to the prepuce orificio which can lead to
scarring and progress to phimosis. Uncircumcised adults
have a risk of secondary phimosis due to loss of skin
elasticity.
1. Bloated tip of the penile prepusium during urination and
can cause urine retention.
2. Disturbance of urine flow in the form of difficult
urination, urine streams shrink, sometimes dripping or
radiating in unexpected directions.
3. Usually babies / children cry and push when urinating
because of pain
4. Hygiene is less clean can cause infection in the prepusium
(postitis), infection of the glans penis (balanitis), or infection
of the glans and prepusium of the penis (balanopostitis).

5. Sometimes the patient is taken for treatment by his parents

because there is a soft lump on the tip of the penis which is
none other than the smegma corpus, the smegma heap in the
sac of the prepusium penis.
 History
In the history usually found complaints in the form of
pubic tip bulging during urination, the disruption of urine flow
in the form of diminished urine stream, babies who cry and
push when urinating because of pain.
 Physical examination
On physical examination of phimosis cases, skin can be
found that cannot be retracted through the penis gland,
corpussmegma, inflammation of the prepusium or on the glans
penis. In physiological phimosis, the preputial orifice has no
wound and looks healthy, whereas in pathological phimosis
there is a circular white fibrous tissue.
1. Parafimosis 3. Balanitis Xerotica Obliterans

2. Balanopostitis
1. Conservative Therapy
As a conservative treatment option corticosteroid ointments
(0.05-0.1%) can be given twice a day for 20-30 days
2. Preputialplasty
3. Circumcision
1. Discomfort or pain when urinating
2. Accumulation of secretions and smegma under the prepuce
which is then exposed to secondary infections and eventually
formed scar tissue.
3. In severe cases can cause urinary retention.
4. Infection of the glans penis (balanitis), prepusium (postitis),
or both (balanopostitis)
5. Urinary tract infections (UTI)
 The prognosis of phimosis will be better if quickly
diagnosed and handled appropriately. There is no record of
long-term aspects of physiological phimosis. If it occurs
after puberty when entering into sexual relations, however, it
can cause disruption of sexual activity.
 The penile retraction prepusium to coronary sulcus
cannot bbe restored to its original state and there
is a bondage to the penis behind the sulcus
 Often in infants and adolescents both those who
have not been circumcised or who have been
circumcised with poor result.
 Pulling the preparation to the proximal wich is
usually done during intercourse/masturbation or
after the installation of catheter but is not returned
to its original place as soon as possible
Attempts to pull teh prepuce behind the shaft to the
penis, especially excessive but fail to return iit to the
front when cleaning the glans penis or when
installing a urinary tube (catheter), can cause
paraphimosis.
pretium skin that cannot return to the fron of the
shaft of the penis will clamp the penis causing a
blood flow dam and sweling (edema) of teh glans
penis and prepuce, even death of the penile tissue
can occur due to obstruction of the arterial blood
flow to the glans penis.
 The prepuce is attempted too be returned
manually by massaging the gland for -5 minutes, so
that the edema is reduced and the prepuce is
slowly returned to its place.
 if the attempt fails, do the dorsum of the incision in
its place after edema and inflamatory process
disappears, the patient is recommended to
undergo circumcision.
 Normally at eight week, the paramesonephric (mullerian)
duct fuses and the uterovaginal septum absorbs. This forms
the fundus and cervix of the uterus and upper one-fifth of the
vaginalis.

 If there is any interruption in the development of the

mullerian duct (such as incomplete development and fusion
of mullerian duct, failure of one or both mullerian duct, failure
of mullerian duct to canalize) would lead to various
anomalies of the uterus.
The American Fertility Society classified classes of congenital
uterine anomalies, include:
1. Hypoplasia/agenesis
2. Unicornuate uterus
3. Didephyls uterus
4. Bicornuate uterus
5. Septate uterus
6. Arcuate uterus

Septate uterus is the most common uterine anomaly with the mean
incidence of about 35%, followed by bicornuate uterus about 26%,
unicornuate uterus about 10%, didelphys uterus about 8%, and the
arcuate uterys is about 20%.
 Uterine anomalies are not symptomatic (that is showing no signs
and symptoms) until the age of puberty when the females with
these anomalies do not menstruate. Doctors who are experts can
diagnose and treat uterine anomalies with the use of developed
imaging techniques such as Hysterosalpingograms (HSG) and
transvaginal ultrasounds in reproductive-aged women.

 A good patient history and clinical examination is key to the

management, because they are usually specific to the
manifestation of the uterine congenital anomaly in the patient.
Factors such as pregnancy loss in a patient’s history and a
bicornuate uterus could be indicated for surgery and
unification.
 One of the most common pediatric disorders of male
endocrine glands &

Most common genital disorder identified at birth.

Cryptorchidism:
A greek word which means ‘hidden testis’
Retractile- 60%
Undescended- 35%
Ectopic- 3%
Ascending- <2%
 DEFINITIONS
Normal scrotal position: positioning of midpointof
the testis at or below midscrotum.

Undescended testis: absence of one or both

testes in normal scrotal position.
 EPIDEMIOLOGY
Cryptorchidism is one of the most
common congenital anomalies.

1% to 4% of full-term and 1% to 45% of preterm male

neonates.
 ETIO-PATHOGENESIS
Multifactorial pathogenesis.
Birth weight is the principal determining factor, at
birth to age one year, independent of the length of
gestation.
Premature infants- 30%
More common in low-birth-weight male newborns,
IUGR, and twin gestation.
 PRESENTATION &
DIAGNOSIS
75% to 80%- palpable and
60% to 70% are unilateral;
involvement of the right side is more common
overall but less frequent in series of nonpalpable
testes.
8% of testes-abdominal, 63% canalicular, 24%
prescrotal, and 11% in the superficial inguinal pouch
or ectopic.
 CLINICAL
FEATURES

Most patients presents in infancy and around school

age.A few present after puberty.

Absence of one or both testes

swelling in the groin (may be the testis or a hernia)

May present with attacks of pain in the groin due either

to recurrent torsion of the testis or strangulation of an
associated hernia.
PHYSICAL EXAMINATION:
Patient should be warm and relaxed for the
examination.
Observation should precede the examination.
Supine and, if possible, upright cross-legged and
standing positions.
Abduction of the thighs contributes to inhibition of
the cremaster reflex.
Document testicular palpability, position, mobility,
size, and possible associated findings such as hernia,
hydrocele, penile size, and urethral position.
 PALPABLE
TESTES
Undescended testes may be located along the line of
normal descent between the abdomen and scrotum or in
an ectopic position.
Ectopic:
 Superficial inguinal pouch(m.c.)
 Perirenal
 Prepubic
 Femoral
 Peripenile
 Perineal
 Contralateral scrotal
 NONPALPABLE
TESTES
When a testis is nonpalpable, possible clinical
findings at surgery include:
1. abdominal or transinguinal “peeping” location
(25% to 50%),
2. complete atrophy (“vanishing” testis, 15% to 40%),
and
3. extra-abdominal location but nonpalpable due to
body habitus, testicular size, and/or limited
pts.’cooperation(10-30%).
Diagnosis of a vanishing testis requires
documentation of blind-ending spermatic vessels in
the abdomen, inguinal canal, or scrotum.

Endocrine evaluation in cases of suspected bilateral

vanishing testis (anorchia) include elevated basal
serum gonadotropin levels and no response to hCG
stimulation.
 CLASSIFICATION

A. Based on palpation (Kaplan-1993)

Impalpable:
High canalicular
Deep inguinal ring
Intra-abdominal
Accounts for 20% of UDT.
Palpable:
Neck of scrotum
Superficial inguinal ring
Low canalicular
Accounts for 80% of UDT
 CLASSIFICATION
CONTD
B. Based on exploration findings:
intra-abdominal
intracanalicular
extracanalicular (suprapubic or infrapubic), or
ectopic.
 INVESTIGATION
Imaging

Abdominal USS
CT Scan
MRI
Because imaging has not been proved to be reliable in
demonstrating whether the testis is present or absent,
its routine use is discouraged
Laboratory Investigations
Karyotyping
↑ FSH- likely represent bilateral anorchia
HCG Stimulation tests- has clinical use where
gonadothrophins are normal
FBC, Urinalysis, Serum electrolytes

Diagnostic Laparoscopy
COMPLICATIONS OF
UNDESCENDED TESTIS
Infertility
Associated hernia
o indirect inguinal hernia usually accompanies a
congenital undescended testis in about 90% cases but
rarely symptomatic.
Testicular atrophy: due to pressure effects and
histological changes.
Trauma
 TREATMENT
GOALS of treatment:
to optimize testicular function,

potentially reduce and/or facilitate diagnosis of

testicular malignancy,

provide cosmetic benefits, and

prevent complications such as clinical hernia or

torsion.
If descent does not occur in the postnatal period
surgical treatment at 6 months of age.
 SURGICAL TREATMENT

Surgery remains the gold standard.

Orchidopexy
Should be performed as early as 6months because of
rarity of spontaneous descent after 6mnths possible
improvement in fertility
Interval of 6months in bilateral undescended testes.
 Principles of orchidopexy
(originally described by Bevan in 1899)

Adequate exposure
Herniotomy
Mobilization of cord
Fixation of testis
 ORCHIDOPEXY FOR THE
PALPABLE UDT
General anesthesia; useful to re-examine the child-
previously nonpalpable testis may become palpable.

groin crease incision is made Careful dissection to

expose the external oblique aponeurosis and the
external ring.
 OUTCOME

Early orchidopexy may improve fertility

No evidence that it reduces risk of malignancy but allows

early identification.