PLENO Kelompok 14 C

3.1
Anggota :
Melinda Tri Agustini (1710311008)
Kelvin Florentino Kaisar (1710311017)
(Minggu 1) Hifzhillah Fajriati (1710311043)
Silvia Rizka (1710312009)
Nur Fatimah Maharani (1710312077)
M. Andhika Dwi Putra (1710313015)
Fatihah Annisa Humaira (1710313033)
Faldo Alfaiza Ramadhan (1710313034)
Aliefia Hidayati Yurizal (1710313054)
Nadhirah Aulia Navis (1710313066)
 Skenario
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?

STEP 1: TERMINOLOGI

1. Skrotum Bifidum : skrotum terbelah dua

2. Hipospadia : muara uretra berada di sisi ventral
penis
3. Mikropenis : ukuran penis kecil dengan ukuran 2,5
cm simpangan baku rata-rata
4. Kordae : pita jaringan fibrosa terbentang pada
bagian ventral penis
5. Gen SRY : factor transkripsi dan gen utama pada
pembentukan penis
6. Karyotyping : metode untuk identifikasi
abnormalitas dari kromosom
STEP 2: IDENTIFIKASI MASALAH

• Mengapa Andi BAK jongkok?

• Bagaimana hubungan penggunaan kontrasepsi hormonal dengan
kelainan yang dialami Andi?
• Bagaimana interpretasi pemeriksaan fisik Andi?
• Apa saja kemungkinan penyebab kondisi Andi?
• Bagaimana penegakkan diagnosis dan tata laksana lanjutan pada
Andi?
• Bagaimana proses organogenesis laki-laki dan perempuan?
• Bagaimana peran gen SRY dalam organogenesis?
• Bagaimana komplikasi yang dapat terjadi dari kondisi Andi?
• Bagaimana investigasi dan cara menentukan jenis kelainan lainnya?
• Bagaimana kemungkinan kelainan urogenital lainnya?
• Bagaimana tata laksana pada Andi?
• Mengapa kasus ini melibatkan multidisiplin dana pa saja
multidisiplinnya?
STEP 3: ANALISIS MASALAH

1. Posisi muara uretra tidak pada ujung glans penis, melainkan

berada di sisi bawah penis atau bagian ventral penis
(hipospadia), di mana terdapat tiga posisi yaitu bagian
anterior, medial, dan posterior sehingga menyebabkan urin
tidak dapat dikeluarkan secara memancar. Hal ini disebabkan
terdapat kelainan pada penutupan uretra yang tidak
sempurna pada masa perkembangannya
2. Kontrasepsi hormonal mengandung hormone progesterone
dan estrogen. Bila ibu meminum obat hormonal dalam
rentan waktu yang pendek dari terjadinya kehamilan, kadar
hormon estrogen dan progesterone pada tubuh ibu
meningkat dan begitupula pada janin, sehingga
mengakibatkan hormone GnRH menjadi sedikit sehingga sel
leydig yang seharusnya menghasilkan testosterone tidak
terbentuk dengan baik. Hormone testosterone yang rendah
mengakibatkan ambiguitas pada organ genital Andi
3 .
Mikropalus: ukuran penis kecil
Kordae: jaringan fibrosa pada penis
Skrotum bifidum: skrotum membelah
Testis teraba unilateral
Merupakan ciri-ciri pada DSD (Disorder of Sexual Development)

4. Tidak diproduksinya gen SRY, kekurangan hormone testosterone, kekurangan hormone

DHT, insensitivitas hormone reseptor, obat hormonal, radiasi, zat kimia, genetic

5. Anamnesis:
– Pada ibu: riwayat obstetric, riwayat minum obat pada kehamilan, riwayat
penggunan KB, riwayat keluarga: kematian neonatus, kelainan organ kelainan pada
saudara kandung, perkembangan pubertas abnormal dan infertilitas pada kerabat
dekat

Pemeriksaan Fisik:
Kondisi umum dan tanda vital: melihat kemungkinan adanya sindrom tertentu
Inspeksi: ada/tidak payudara, panjang falus, lipatan labioskrotal, adanya
hiperpigmentasi, derajat prader
Palpasi: gonad teraba/tidak
Pemeriksaan Penunjang: radiologi pelvis & abdomen, karyotyping, analisis gen SRY, kadar
hormone testosterone & DHT, kadar hormone FSH dan LH
6
• TDF: Testis Determination Factor (gen SRY, terdapat pada
kromosom Y) untuk membentuk testis
• MIF: Mullerian Inhibitor Factor (Anti Mullerian Hormone) dihasilkan
oleh sel sertoli
• Testosteron: dihasilkan oleh sel leydig

7 Terjawab pada analisis masalah nomor 6

8 Gangguan ejakulasi dan infertilitas. Hal ini disebabkan testis tidak

berada di tempat yang seharusnya sehingga tidak berada pada suhu
optimal, mengakibatkan sperma tidak dapat dihasilkan atau
kualitasnya tidak baik
9
• Dengan pemeriksaan penunjang
• Karyotyping: melihat adanya kelainan kromosom/tidak
• Analisis gen SRY: apakah kromosom XY memiliki gen SRY
• Radiologi abdomen dan pelvis: melihat kelainan urogenital
bawaan lainnya
10
Pembentukan sistem urogenital saling mempengaruhi antar
organnya sehingga tidak menyingkirkan kemungkinan adanya
kelainan pada organ lainnya. Dapat ditemukan adanya
ovarium (hermafrodit), agenesis testis, dll. Maka dari itu
diperlukan pemeriksaan penunjang untuk menegakkan
diagnosisnya
11 Pembedahan untuk memindahkan testis ke tempat yang
seharusnya, hormonal untuk perkembangan genitalnya
12 Melibatkan bedah, anak, dan psikolog
Classification of Urogenial
Congenital Disorder
Kidney VesicoUretra
1. Renal Agenesis 1. Extrofia Buli-buli
2. Supernumery Kidneys 2. Urachus Persistent
3. Renal Ectopic 3. Vesicouretra Reflux
4. Renal Hypoplasia 4. Hypospadia
5. Horshoe Kidney 5. Epispadia
6. Policystic Kidney 6. Megalourethra
7. Double Ureter 7. Congenital Uretra
Fistule
Gonad Genitalia Externa
1. Agenesis Testis 1. Fimosis
2. Ectopic Testis 2. Parafimosis
3. Cryptochismus 3. Micropenis
4. Burried Penis
5. Webbed Penis
6. Aphalia
7. Ambigus Genitalia
8. Hymen Imperforata
Ectopic Kidney
• Ectopic kidneys are misplaced from their
normal location sublumbar because of
abnormal migration during fetal development.

• Often ectopic locations include the pelvic

cavity or inguinal position
 INCIDENT

• Found no differences in gender in ectopic

kidneys, incidence 1: 900 of the population.
Some say 8.3 to 11: 10.000, equally in both
sexes, Ectopic pelvic kidney is the most
commonly found around 60% of all
occurrences of ectopic kidney.
 ETIOLOGY

• Failure shoots migration and development

metanephric blastema ureter into the renal
fossa. Factors affecting the development of
such a teratogen, genetic factors, maternal
diseases affecting the ureter and metanefrik
buds can cause the displacement of abnormal
kidney and kidney etopik
 DIAGNOSIS

A. CLINICAL
• usually asymptomatic unless complications
such as ureteral obstruction or severe
infection. Symptoms usually appear as: lower
abdominal pain (discomfort), dysuria,
micturition frequen and hematuria, Proteinuri,
can be discovered during a routine
examination.
 DIAGNOSIS

• • Nephroptosis
• • agenesis ren
• • A tumor in the pelvic cavity
• • Duplication of the collecting system.
• ,
 TREATMENT

• Ectopic kidneys treated in case of obstruction or

vesicoureteral reflux. If there is no severe damage at
the time of the discovery of these disorders,
obstruction may be reduced or Vur corrected with
surgery. When it is happening scar the kidneys and
the kidneys can no longer work properly, then the
removal of the kidney may be the best option.
• The surgical procedure is most often used in an
ectopic kidney stone removal include, pieloplasti,
correction reflux, and nephrectomy.
 PROGNOSIS

• Well, if there are no other serious disorders or

chromosomal disorders that accompany. On
the other healthy neonates, renal pelvis
associated with an increased risk of secondary
hidronephrosis that can change the course of
the ureter. ,
Horseshoe Kidney
 Horseshoe kidneys

• Most common of all renal fusion anomalies

• Occurs in 0.25% of the population

• fusion occurs before the kidneys have rotated on

their long axis
The lower poles of the two kidneys touch and fuse as they cross the iliac arteries
• In 95% of patients, the kidneys join at the lower pole; in a
small number, an isthmus connects both upper poles instead

• Calyces normal in number, are atypical in orientation

• Ureter may insert high on the renal pelvis and lie laterally

• Blood supply to the horseshoe kidney can be quite variable

Arteriogram showing a multiplicity of arteries supplying kidney arising from
aorta and common iliac arteries
• UPJ obstruction, causing hydronephrosis, occurs in
one third of individuals

• 60% patients remain asymptomatic for aprox. 10

years
Associated Anomalies
 Diagnosis
• Excretory urogram
 Prognosis
• 13% have persistent urinary infection or pain

• 17% develop recurrent calculi

• Renal carcinoma has been reported within a horseshoe

kidney in 123 patients

• Incidence of Wilms' tumor in horseshoe kidneys is more

than twice
Hispopadia
HIPOSPADIA
Hypospadias is a congenital deformity where the opening of
the urethra
(the meatus) is sited on the underside (ventral) part of the
penis, anywhere
from the glans to the perineum. It is often associated with a
‘hooded’ foreskin
(prepuce) and chordee (ventral curvature of the penile shaft).
It occurs
in 1 in 250 live ♂ births, and the incidence is increasing. There
is an 8% incidence
in offsprings of an affected ♂ and a 14% risk in ♂ siblings.
Risk is i
in offspring of very young and older mothers and in low-
birthweight babies.
 Tatalaksana
Hipospadia
Anak dengan hipospadia sebaiknya jangan
disirkumsisi dahulu  preputium
dibutuhkan untuk rekonstruksi urethra
Sebaiknya hipospadia ditatalaksana
sebelum usia 3 tahun (alasan psikologis)

Tujuan utama
• Orthoplasti & release chordee (chordektomi) 
meluruskan kembali penis dan mengembalikan
kurvatura penis
• Urethroplasty  rekonstruksi urethra supaya OUE
bisa di ujung glans penis
• Glansplasty  membentuk kembali konfigurasi glans
penis
Fimosis & Parafimosis
 FIMOSIS

• Definisi : prepusium penis yang tidak dapat di

retraksi ke proksimal sampai korona glandis

• Epidemiologi : dialami sebagian besar bayi

baru lahir karena terdapat adhesi ilmiah
antara prepusium dengan glands penis, seiring
bertambahnya usia adhesi tersebut mulai
terpisah
• Fisiologis
usia 3-4 tahun penis tumbuh dan berkembang
Debris epitel2 prepusium yang mengalami
deskuamasi oleh bakteri  smegma
Smegma mengumpul di dalam prepusium
Memisahkan prepusium dari glands
Ereksi penis berkala membantu Prepusium
terdilatasi perlahan
Prepusium menjadi retraktil
Dapat ditarik ke proksimal pada usia 4 tahun
(90% anak)
• Patofisiologis

pada sebagian anak, prepusium tetap menempel

pada glands
Ujung prepusium menyempit
Tumpukan smegma >> benjolan lunak di ujung
penis
Gangguan fungsi miksi  sulit kencing pancaran
urin kecil urin terkumpul di sakus prepusium 
ujung penis tampak menggelembung
Kurangnya higiene dapat menyebabkan infeksi pada
prepusium (postitis), glands (balanitis), atau keduanya
(balanopostitis)
• Penatalaksanaan
– Salep dexamethasone selama 1-2 bulan
– Dorsal slit
– sirkumsisi
• Tidak boleh dilakukan retraksi paksa
– Karena dapat menimbulkan sikatriks dan fimosis
pathologis
 PARAFIMOSIS
• Definisi : prepusium penis yang di retraksi
sampai di sulkus koronarius tidak dapat
dikembalikan pada keadaan semula dan timbul
jeratan pada penis di belakang sulkus → mrp
• Etiologi : retraksi prepusium ke proksimal
yang biasa terjadi pada saat koitus, masturbasi,
atau pada pemasangan kateter
• Epidemiologi : sering pada bayi dan remaja,
baik yang belum sirkumsisi atau yang sudah
sirkumsisi dengan hasil yang kurang baik
• Patofisiologi

Retraksi prepusium ke proksimal secara

berlebihan
Tidak dapat dikembalikan ke depan batang penis
Menjepit penis (jeratan)
Mengganggu aliran balik vena superfisial
Bendungan aliran darah
Edema dan nyeri
Jika dibiarkan lama dapat terjadi nekrosis glands
penis
• Penatalaksanaan
– Mengembalikan prepusium secara manual dengan
cara memijat glands 3-5 menit untuk mengurangi
edema
– Jika tidak berhasil lakukan dorsum insisi pada
jeratan
– Setelah edema dan inflamasi hilang, lakukan
sirkumsisi
SIRKUMSISI
1. Pasien dlm posisi supine , pada bayi dgn anestesi lokal, sedangkan pada anak yg
lebih besar dgn general anestesi
2. Asepsis dan antisepsis prosedur
3. Dilakukan pembersihaan smegma dengan membuka preputium perlahan2
4. Preputium dikembalikan ke posisi semula
5. Klem preputium pada arah jam 11, 1 dan 6
6. Dilakukan dorsal split pada arah jam 12 sampai corona glandis
7. Lakukan jahit kendali mukosa – kulit pada arah jam 12
8. Gunting preputium secara melingkar dgn menyisakann frenulum pada klem jam
6
9. Lakukan ligasi pada perdarahan
10. Dilakukan penjahitan interupted dgn benang absorbable 4.0 pada jam 3, 6, 9
dan 12
11. Jahit angka 8 pd frenulum, lakukan pemotongan frenulum di distal jahitan
12. Kontrol luka dan jahitan, oleskan antibiotik
13. Balut dgn kasa steril
Undescended Testis /
Cryptorchidism
DEFINITION
• Cryptorchidism comes from the word cryptos
(Greek) which means hidden and orchis (latin)
which means testis.
• Cryptorchidism is a condition where after one
year of age, one or two testicles are not in the
scrotal sac, but are in one place along the
normal testicular descent.
 CLASSIFICATION
Based on etiopathogenesis:
a. Mechanical / anatomic: attachment,
inguinal canal abnormalities
b. Endocrine / hormonal: hypothalamic-
pituitary-testicular abnormality
c. Dysgenesis: multiple intersex
abnormalities
d. Hereditary / genetic
Based on location:
- High scrotal (supraskrotal): 40%
- Intrakanalikuli (inguinal): 20%
- Intraabdominal (abdomen): 10%
- Obstruction: 30%
EPIDEMIOLOGY
• The incidence of UDT is different in each age.
• Newborns (3-6%), one month (1.8%), 3 months (1.5%), One year
(0.5 - 0.8%). Babies born at just 3% of them are cryptorchid, while
births are about 33% less.
• At birth weight (BBL) under 2000 grams the incidence of UDT was
7.7% BBL 2000-2500 (2.5%), and BBL above 2500 (1.41%).
• The incidence of unilateral cryptorchidism is higher than bilateral
cryptorchidism.
• While the incidence of the left side was greater (52.1% left vs 47.9%
right). In the United Kingdom, the incidence increased by more than
50% in the period 1965 - 1985.
• FKUI - RSUPCM from 1987 - 1993 there were 82 cryptorchid
children, while in FKUSU - RSUP. Adam Malik Medan during the
period 1994 - 1999 there were 15 cases.
ETIOLOGY
• Testicular gubernaculum abnormalities
• Testicular intrinsic defect
• Deficiency of hormonal / endocrine
stimulation
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 birth (twins 2, twins 3)
• Premature birth (gestational age less than 37
weeks)
• Fetal weight under the age of pregnancy
• Have a father or relative with a history of UDT
DIAGNOSIS
 History
 Physical examination
• Determination of testicular location
• Determination of whether the testicles are palpabel
 Supporting investigation
Done if the testicles are impalpable or doubt some
supporting modality is needed.
• Ultrasonography (USG)
• CT scan
• MRI
MANAGEMENT
• The objectives of handling UDT are:
• Increase vertility
• Prevents testicular torsion
• Reducing the risk of injury, especially if the testis
is located in the pubic tubercle
• Correcting other disorders that accompany, such
as hernias
• Prevents / early detection of testicular malignancy
• Establish a body image
NON SURGICAL THERAPY
• HCG
• LHRH
• HCG LHRH combination

Evaluation of therapy
• By time: end of injection, 1 month, 3 months, 3 months, 6 months
and 12 months.
• Based on position: complete response when the testis is in the
scrotum, while incomplete response when the testis is inferior to the
inguinal position Side effects are reversible. The term abnormalities
in the form of increased testicular size, penis enlargement, erections,
increased scrotal rugosity, growth of pubic hair hyperpigmentation
and emotional disturbances.
 SURGICAL THERAPY
Surgical indications:
• Hormonal therapy failed
• A hernia has the potential to cause complications
• Suspected testicular torsion
• Intraabdominal location or above the inguinal
canal
• Ectopic testes

Stages: one stage or 2 stages depending on the

spermatic vasa whether long or short.
Standard Orchydopexy
• The principle of orchidopexy includes 3 stages
• Funiculolysis
• Transfer of the testes into the scrotum (transposition)
• Fixation of the testes in the scrotum

• Stephen Flower Orchidopexy

Is a standard orchidopexy modification. When the testicular arteries
do not reach the scrotum long enough, the testicular arteries are
ligated. So the testes only rely on the vas deferens arteries.

• Orchydopexy bertahap
Surgery: The testicles are wrapped in silastic sheets and fixed to the
pubis in stage I. After 6-8 months a phase II of exploration and
inserting the testes into the scrotum is performed.
Laparoscopy: Clamping the testicular arteries with laparoscopy is
done in stage I for abdominal type UDT. After 6-8 months, Stephen
Flower Orchydopexy worked on it.
 COMPLICATIONS
Pre Operative
• Inguinal hernia
• Torsion Testis
• Testicular trauma
• Malignancy
• Infertility
• Psychological

Post Operative
• Infection
• Testicular atrophy
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%.
Testicular Torsion
DEFINITION

Testicular torsion is an emergency in the

form of rotation of the longitudinal axis of
the spermatic cord which results in blocked
testicular blood flow. Most acute cases of
scrotum in children are testicular torsion.
EPIDEMIOLOGY
Testicular torsion is the most common cause of acute
scrotum. The incidence of testicular torsion is 1 in
4000 men before the age of 25 years. Testicular
torsion can occur at any age, most often at the age of
12-16 years; the left side more often. The median age
of testicular torsion patients is 15 years.
CLASSIFICATION

Testicular torsion according to the cause is divided into

extravaginal and intravaginal.
Testicular torsion is also divided according to its duration
since onset. The division is also clarified with pathological
features on sonographic examination :
- Type 1 -> Acute phase
- Type 2 -> Initial phase
- Type 3 -> Late phase
RISK FACTORS
- Season with lower and humid temperatures like spring and
cold
- Pregnancy with complications such as prolonged labor, pre-
eclampsia, gestational diabetes, multiple pregnancies, large
birth weight, and vaginal delivery
- family history, Cryptorchidism or undescended testicles are
also said to increase 10 times the risk of testicular torsion.
PATHOPHYSIOLOGY
Intravaginal and extravaginal torsion will result in testicular
ischemic injury due to the spin of the testis in the spermatic
cord pediculus. Experimental studies show that testicular
infarction begins 2 hours after the onset of testicular
torsion, irreversible damage occurs after 6 hours, and
complete infarction arises at 24 hours.
Intravaginal
The cause of intravaginal testicular torsion is an anatomical
abnormality in the form of tunica vaginalis that covers the
entire testis and epididymis so that the attachment to the
scrotum is disrupted.
This deformity is better known as the "bell clapper" which is
characterized by increased testicular mobility. Intravaginal
testicular torsion most often occurs during sleep, and due
to trauma.
Extravaginal
Extravaginal torsion of the testis is most common
in cases of fetal and neonatal torsion. In this type
of torsion, spermatic cord twisting occurs outside
the tunica vaginalis sac in the scrotum. The
external spermatic fascia is not attached to the
dartos muscle, and new spermatic cord attaches
to the scrotum in 7-10 days of life.
APPEAL DIAGNOSIS

Testicular torsion is often misdiagnosed; Testicular torsion is the 3rd

most common malpractice case in adolescents aged 12-17 years. The
most common misdiagnosis is epididymitis.
In children it is important to be distinguished from appendicitis,
hematocele, hydrocele, testicular neoplasms, and scrotal abscesses
whose symptoms are similar to torsion.
What distinguishes the torsion of the testicular appendix from the
testicular torsion, in addition to its gradual complaints, is the presence
of a blue dot sign that is commonly found in the anterosuperior region
of the testis.
DIAGNOSIS
a. Anamnesis

Severe unilateral pain that is suddenly felt at rest and

is often accompanied by nausea, vomiting. Nausea,
vomiting caused by celiac ganglion stimulation
reflexes, is an important symptom of ischemic
systemic effects in the body.
b. Physical examination
On physical examination found tenderness, abnormal testicular
position, and loss of cremaster reflexes. Abnormal testicular position
occurs because the spermatic cord is shortened, twisting will pull the
testis higher.
• Cremaster reflex examination
- positive results: good testicular blood flow
- negative results: there is twisting
Edema, induration, and scrotal erythema can be found in severe
degrees.
• Examination of Phren's sign is important to distinguish pain caused
by torsion or orchitis.
Torsion position can be touched on physical examination. The cord knot
is palpated by identifying the top of the testis and the head of the
epididymis.
Enlargement of the painful and hard left scrotum
c. Radiology Examination

The most important are Doppler ultrasound (DUS)

and Radionuclide Scrotal Imaging (RNSI) to assess
testicular perfusion and whether the testis is viable.
Color DUS shows "spiraling" (whirlpool) or twisting
of vessels on the spermatic cord topography.
a) Scrotal ultrasound describes
the position of the left testicle
which is abnormally tranverse
with minimal reactive
hydrocele.

b) Doppler ultrasound shows

the least blood flow to the left
testis.
 TREATMENT
a. Manual Detortion : Detection manually is done by intravenous sedation or
spermatic cord anesthesia. The success of a detortion is marked by the loss
of pain complaints. Even though manual detortion is successful, operative
action is required, namely immediate orchidopexy, and biopsy examination.

b. Surgical Exploration: Surgical exploration continues in all cases of testicular

torsion. In exploration, a spermatic and testicular heavenly derotation was
performed, along with an assessment of testicular viability after detortion.
Orchidectomy if the testicles are necrotic and non-viable. Orchidectomy is
performed by contralateral testicular orchidopexy. If the testis is viable
after detortion, bilateral orchidopexy is performed. In paradise exploration,
1/3 of the torsion testis cases were found dead and had an orchiectomy. In
the saved testicles, testicular damage is still found accompanied by a
decrease in testicular size. Anti-sperm antibody examination and inhibin B
can be used as markers of testicular function after surgery. After
exploration or detortion, the testes are covered with warm gauze for 10-15
minutes and assess for signs of testicular reperfusion.
The spermatic cord
twists on the
testicular torque
 PROGNOSIS
- Infertility is a long-term consequence
- Impaired spermatogenesis due to torsion of the testes will reduce
sperm quality.
The sooner the diagnosis is established, <6 hours, the better
the prognosis can be saved of the testes. The most common cause of
orchidectomy is late diagnosis. The orchidectomy rate is 9% at <6 hours
after onset and 56% at> 6 hours. Testicular ischemia will result in
testicular atrophy. After torque, 36-39% of men will have a sperm
concentration below 20 million / mL.
In the perinatal age group, the testes can no longer be saved,
whereas in the postnatal age group immediate paradise exploration is
needed. Recurrent torsion can occur several years after orchidectomy
and orchidopexy.
 CONCLUSION
Testicular torsion is an emergency case in children
and adolescents. A quick and precise diagnosis is
needed because the speed of the intervention
greatly affects the safety of the testes. Doppler
ultrasound is still the choice for diagnosis of torsio
testis. The only treatment is detortion. Although the
most ideal is surgical detortion, clinicians must know
the technique of manual detortion.
Congenital Adrenal
Hyperplasia (CAH)
Definition
Congenital adrenal hyperplasia (CAH) is a family of
inherited enzyme deficiencies (21-hydroxylase
deficiency ) that impair normal corticosteroid
synthesis by the adrenal cortex.

Epidemiology
The estimated prevalence is 1/10,000 and annual
incidence ranges from 1/5,000 to 1/15,000.
Etiology
• In 90-95% of cases, CAH is caused by a mutation
in the CYP21A2 gene located on chromosome
6p21.3 which encodes for an enzyme that
controls cortisol and aldosterone production.
Patophysiology
Clinical Manifestation
Diagnosis
• Prenatal testing
Tests to diagnose CAH in fetuses can be done
when siblings have the disease or family members
are known to carry the gene defect. One of these
tests may be done:
1. Amniocentesis. This procedure involves using a
needle to withdraw a sample of amniotic fluid
from the womb, and then examining the cells.
2. Chorionic villus sampling. This test involves
withdrawing cells from the placenta for
examination.
• Newborns, infants and children

1. Physical exam. The doctor examines your child and evaluates

symptoms. If, based on these findings, the doctor suspects CAH,
the next step is to confirm the diagnosis with blood and urine
tests.
2. Blood and urine tests. Tests used to diagnose CAH measure levels
of hormones produced by the adrenal glands. A diagnosis can be
made when there are abnormal levels of these hormones.
3. Gene testing. In older children and young adults, genetic testing
may be needed to diagnose CAH.
4. Testing to determine a child's sex. In female infants who have
severe ambiguous genitalia, tests can be done to analyze
chromosomes to identify genetic sex. Also, pelvic ultrasound can
be used to identify the presence of female reproductive
structures such as the uterus and ovaries.
Treatment
• ACTH suppressor with steroid
– Hydrocortisone
– Mineralocorticoid (salt losing)
– Genitoplasty on 3-6 months
– Adrenalectomy on severe cases which is hard to
suppress the adrenal
THANKS