TESTICULAR TORSION

Dr. Hari Krismanuel, Sp. B, FInaCS

PROBLEM
SEORANG LELAKI 17 TH, PELAJAR SMU, BELUM MENIKAH, NYERI DI KANTONG PELIR DATANG KE UGD JAM 06.30.

HYPOTHESIS ? MECHANISM ? MORE INFO ?

SYMPTOMS & SIGNS

ANAMNESA : WHAT, WHERE, WHEN, WHY, HOW ? PHYSICAL EXAMINATION

Differential Diagnosis
Note: This table describes typical features. In practice it is often difficult to be certain of the diagnosis clinically ie. sometimes the diagnosis may only be made by surgical exploration. Diagnosis Torsion of the testis Suggestive features on history Sudden onset testicular pain and swelling; occasionally nausea, vomiting. Note: pain may be in the iliac fossa More gradual onset of testicular pain Suggestive features on examination Discolouration of scrotum; exquisitely tender testis, riding high Focal tenderness at upper pole of testis; "blue dot" sign necrotic appendix seen through scrotal skin Note: Difficult to distinguish from testicular torsion Red, tender, swollen hemiscrotum; tenderness most marked posteriolateral to testis. Pyuria may be present. Firm, tender, irreducible, inguinoscrotal swelling Bland violaceous oedema of scrotum, extending into perineum + penis; testes not tender Soft, non-tender swelling adjacent to testis; transilluminates brightly. may be difficult to distinguish from testicular torsion in absence of other features

Torsion of the appendix testis (hydatid of Morgagni) Epididymoorchitis

Onset may be insidious; fever, vomiting, urinary symptoms; rare in pre-pubertal boys, unless underlying genitourinary anomaly, when associated with UTI. History of intermittent inguinoscrotal bulge, with associated irritability Swelling noted but child not distressed Swollen hemiscrotum in well, settled baby Painful scrotal oedema, with purpuric rash over scrotum. May have associated vasculitic rash of buttocks and lower limbs, arthritis, abdominal pain with GI bleeding, and nephritis

Incarcerated inguinal hernia Idiopathic scrotal oedema Hydrocele Henoch Schonlein purpura

Testicular or epididymis rupture

Scrotal trauma eg. straddle injury, bicycle handlebars, Tender swollen testis. Bruising, oedema, haematoma, sports injury. Delayed onset of scrotal pain and or haematocele may be present. swelling.

ANAMNESA
WHAT : - NYERI HEBAT SKROTUM KIRI, SAMPAI TERBANGUN DARI TIDUR WHERE: - PADA SKROTUM KIRI

WHEN : - SEJAK 3 JAM LALU

HOW : - NYERINYA MENETAP, TIDAK BERUBAH DENGAN PERUBAHAN POSISI - SAAT INI SEMAKIN NYERI (BERTAMBAH) - SKROTUM KIRI BENGKAK, NYERI TEKAN, MASSA DALAM SKROTUM KIRI SEJAK 1 JAM LALU, - MUAL (+) , MUNTAH (-) WHY : - NYERINYA MENDADAK, SEBELUMNYA TIDAK ADA KELUHAN INI - KELUHAN MIKSI DAN BAB (-) , DEMAM (-) - RIWAYAT TRAUMA (-) , RIWAYAT HUBUNGAN SEKS (-) - RIWAYAT KELUARGA (-) , RIWAYAT ALERGI (-) , GGN. PERDARAHAN (-)

PHYSICAL EXAMINATION
STATUS INTERNUS : - KEADAAN UMUM TAMPAK KESAKITAN, LAIN LAIN DALAM BATAS NORMAL

STATUS LOKALIS SKROTUM : INSPEKSI : - BESAR SKROTUM : KIRI > KANAN - KULIT SKROTUM : ERITEMA , EDEMATOUS , SKIN PITTING PADA DASAR SKROTUM - TANDA TANDA TRAUMA (JEJAS) TIDAK ADA - TESTIS KIRI LEBIH TINGGI DARI TESTIS KANAN PALPASI : - TESTIS KIRI > TESTIS KANAN - KONSISTENSI TESTIS KIRI KERAS , PADAT - NYERI TEKAN TESTIS KIRI - NYERI TIDAK BERKURANG SAAT TESTIS KIRI DIANGKAT - AKSIS TESTIS KIRI LEBIH MENDATAR / HORISONTAL - BATAS TESTIS DAN EPIDIDIMIS KIRI TIDAK JELAS - SPERMATIC CORD MEMBESAR , MENEBAL DAN NYERI TEKAN - REFLEKS KREMASTER KIRI (-) - FINGER TEST (-) - DIAFANOSKOPI / TRANSILUMINASI : (-)

PATHOGENESIS
Testicular torsion: (A) extravaginal; Occur perinatally, during testicular descent and prior to testicular fixation in the scrotum . These comprise 5% of all testicular torsions . In the neonatal age group, the testicle frequently has not yet descended into the scrotum, where it becomes attached within the tunica vaginalis. Incomplete fixation of the gubernaculum to the scrotal wall allows the entire testes and tunica free rotation within the scrotum. Typically occurs within the first 7-10 days of life. The rotation of the cord is proximal to the attachment of the tunica vaginalis that encloses the testes.

Testicular torsion: (A) extravaginal; (B) intravaginal.

PATHOGENESIS
Testicular torsion: (B) Intravaginal ; Most often is observed in males younger than 30 years, with most aged 12-18 years. The peak age is 14 years. Occurs in the remaining 95% of all testicular torsions. A congenital high attachment of the tunica vaginalis on the spermatic cord allows the testes to rotate freely on the cord, within the tunica vaginalis. This congenital anomaly, called the bell clapper deformity, results in the long axis of the testicle to become oriented transversely rather than cephalocaudal. It is present in approximately 12% of males, 40% of which have the abnormality in the contralateral testicle as well. A large mesentery between the epididymis and the testis can also predispose itself to torsion, although this is rare. Contraction of the spermatic muscles shortens the spermatic cord and may initiate testicular torsion.

PATHOGENESIS
Causes Congenital anomaly ; bell clapper deformity Undescended testicle Sexual arousal and/or activity Trauma Exercise Active cremasteric reflex Cold weather Risk Factors Trauma (only responsible for 4-8% of cases) Vigorous Exercise Prior episode of similar pain spontaneously resolved Testicular hypertrophy during Puberty Testicular mass Cryptorchidism (status-post repair) Long intrascrotal length of vas deferens

PATHOPHYSIOLOGY
Normally, the tunica vaginalis attaches to the posterolateral surface of the testicle and allows for little mobility of the testicle within the scrotum. In patients who have an inappropriately high attachment of the tunica vaginalis, the testicle can rotate freely on the spermatic cord within the tunica vaginalis (intravaginal testicular torsion), causing venous occlusion and engorgement, with subsequent arterial ischemia causing infarction of the testicle. Increasing testicular and epididymal congestion promotes progression of torsion. In the neonatal age group, the testicle frequently has not yet descended into the scrotum, where it becomes attached within the tunica vaginalis. This mobility of the testicle predisposes it to torsion (extravaginal testicular torsion). Inadequate fusion of the testicle to the scrotal wall, moreover, typically occurs within the first 7-10 days of life. Ischemia / tissue injury results in the release of inflammatory mediators (cytokines) from damaged cells, increasing the transduction of painful stimuli. In addition to local cellular events, potassium, prostaglandins, bradykinins, ATP and other mediators from damaged cells trigger the nociceptors to send afferent impulses via the dorsal root ganglion to the spinal cord. Afferent information is transmitted via second-order neurons in the dorsal horn through the spinothalamic tract to the thalamus and to the sensory cortex . These higher centres are responsible for the perception of pain.

PATHOPHYSIOLOGY

Inflammatory cytokines act on and between inflammatory cells, inducing some of the features of the inflammatory response. Testicular torsion results in a high-riding testis (Demming sign) with an abnormal (transverse) lie (Brunzel sign) may suggest torsion. In early torsion, the entire testis is swollen and tender, and is larger than the unaffected testis. The normal separation of the testis from the epididymis may not be palpable for only a few hours. The spermatic cord is typically thickened and tender. Typically, no pain relief occurs with scrotal elevation (negative Prehn sign), as observed with acute epididymitis. Discrepancies in size, degree of swelling, presence and location of erythema, thickening of the scrotal skin. Skin pitting at the scrotal base (Ger sign) may provide evidence in support of the diagnosis.

OPTION OF MANAGEMENT
SYMPTOMS & SIGNS HYPOTHESIS & MECHANISM

DIAGNOSA COST / RISK BENEFIT

THERAPY COST / RISK

LAB / IMAGING STUDY

CONSULTATION BENEFIT

THERAPY CONSULTATION GIVE THE PROPER MANAGEMENT FOR PATIENTS SAFETY

TESTICULAR TORSION HIGHLIGHTS

Must not miss diagnosis The acute scrotum is a true urologic / surgical emergency. The window of opportunity to salvage a torsed, ischemic testicle is only 6 hours. Acute scrotal swelling should be considered testicular torsion until proven otherwise. Early surgical consultation is vital, as delay in scrotal exploration and detorsion of a torted testis will result in testicular infarction within 8-12 hours. Keep the patients fasted.
A salvage rate of 100% is found in patients who undergo detorsion within 6 hours of pain; Delay of more than 6-8 hours between onset of symptoms and the time of detorsion reduces the salvage rate to 55-85%; 20% viability rate if detorsion occurs after 12 hours; and 0% viability if detorsion is delayed greater than 24 hours. A correlation may exist between the duration of torsion and abnormal semen parameters, and some authorities suggest that retention of an injured testis can induce pathologic changes to the contralateral testis.

TESTICULAR TORSION HIGHLIGHTS

The suspicion of testicular torsion requires immediate surgical intervention to provide testicular salvage. Detorsing of the involved testis, with bilateral orchiopexy, is the standard surgical approach. Testicular fixation performed with permanent suture. This treatment is preferred because of the subsequent increased risk of future contralateral torsion. If the testicle is nonviable, orchiectomy is usually performed. Many patients with classic symptoms and signs of torsion require no imaging corroboration. If testicular torsion is clinically suggested, perform immediate surgical exploration, regardless of laboratory studies because a negative finding upon exploration of the scrotum is more acceptable than the loss of a salvageable testis. The salvageability of a testicle within 6 hours of torsion is very good. Greater than 6 hours is more worrisome, but exploration should be performed to remove a necrotic testicle, even with a late presentation, as diminished fertility may result from leaving in an infarcted testicle

CORRELATION BETWEEN TESTICULAR TORSION AND DECREASED FERTILITY

Recent studies show that exocrine and endocrine function is substandard in men with a history of unilateral torsion. The following 3 theories explain the contralateral disease noted in torsion: - Unrecognized or unreported repeated injury to both testes - Preexisting pathologic condition predisposing to both abnormal spermatogenesis and torsion of the spermatic cord - Induction of pathologic changes in the contralateral testis by retention of the injured testis To explain the decreased fertility observed in unilateral torsion of the spermatic cord, several specialists suggest an autoimmune mechanism. This hypothesis is based upon the following: - Knowledge of the blood-testis barrier, which isolates the luminal compartment of the seminiferous tubule - Inducing experimental allergic orchitis - Likening contralateral testicular disease to sympathetic ophthalmia, a cell-mediated immune response

MANAGEMENT
Patient with Acute Scrotum
History , physical examination

Short duration on symptoms and high probability of torsion

Long duration of symptoms and low probability of torsion

Surgical Exploration

Color Doppler Ultrasonography

Decreased or absent blood flow

increased or normal blood flow or equivocal results. non operative management or observation

Surgical exploration

LABORATORY STUDIES
A CBC and urinalysis are normal (this results in an unnecessary delay of one hour). In general, laboratory tests are not diagnostically useful in distinguishing torsion from other acute scrotal syndromes. Urinalysis Urinalysis result is usually normal. The presence of white blood cells (WBCs) can be observed in as many as 30% of patients who have torsion; therefore, do not rely on WBC presence to exclude the diagnosis. Complete blood count: CBC can be normal or show an elevated WBC count in as many as 60% of patients who have torsion. Acute-phase proteins (C-reactive protein [CRP]): Elevation in acute-phase proteins, namely the CRP, has been postulated as a diagnostic aid in differentiating inflammatory causes of acute scrotal pain (epididymitis) from noninflammatory causes (testicular torsion). However, sample sizes in these studies have been too small to definitively rule out testicular torsion using CRP as a diagnostic adjunct. If testicular torsion is clinically suggested, perform immediate surgical exploration, regardless of laboratory studies because a negative finding upon exploration of the scrotum is more acceptable than the loss of a salvageable testis.

IMAGING STUDIES
Imaging studies may be useful when a low suspicion of testicular torsion exists Color Doppler ultrasound scanning of the scrotum Use high frequency transducer Testicular torsion : 1. Enlarged affected testicle 2. Absent arterial and venous flow to the affected testicle and epididymis. 3. Increased RI on affected side (diminished or reversed diastolic flow) 4. Decreased flow velocity difficult to measure because of small vessels/ angle correction but may be subjectively inferred by relative difficulty in finding small, low-amplitude flow on symptomatic side 5. No testicular masses are noted. Absence of blood flow to the affected testicle is noted in testicular torsion, whereas increased blood flow is noted in epididymitis/orchitis. Flow to the testicle will be present in appendage torsion. Of course, these findings should be combined with the signs and symptoms, and not taken in isolation. Testicular anatomy is also appreciated with ultrasound, helping to evaluate for testicular rupture, hematomas, and tumors. Nuclear testicular scan Nuclear testicular scan can help differentiate torsion from acute epididymitis by demonstrating cold spot and ring signs.

WHY NEED IMMEDIATE SURGICAL CONSULTATION ?

Indication :
The window of opportunity to salvage a torsed, ischemic testicle is only 6 hours. Early surgical consultation is vital, as delay in scrotal exploration and detorsion of a torted testis will result in testicular infarction within 8-12 hours. Success in the management of spermatic cord torsion is measured by immediate testicular salvage and incidence of late testicular atrophy, which are, in turn, directly related to the duration and degree of testicular torsion. Delaying surgical intervention worsens the intraoperative testicular salvage and incidence rate and the extent of subsequent testicular atrophy.

Complications :
Infarction of testicle Loss of testicle Infection Infertility secondary to loss of testicle Cosmetic deformity

No testicles mean no erection

Men who have lost both of their testes may experience a reduction in sex drive and difficulty in getting and/or maintaining an erection (impact on their sex life).

MEDICAL / LEGAL PITFALLS

Failure to recognize a surgical / urologic emergency Delay in obtaining surgical / urologic consultation Misdiagnosing as epididymitis / orchitis Partial reduction of a torsion (ie, 720)