Testicular torsion is a true urologic emergency. It occurs when
a testicle rotates on its vascular pedicle resulting in vascular
obstruction (Figure 130-1). Torsion is most common between the ages
of 12 to 18.1 Age should not be considered when making
the diagnosis, however, as torsion may occur in an antenate, neonate,
or geriatric patient.2A history
of prior orchiopexy does not negate the possibility of torsion. Presenting
signs and symptoms frequently include acute and diffuse scrotal
pain, scrotal swelling, a high-riding testicle, and an absent cremasteric
reflex. If torsion is suspected, a Urologist
should be consulted immediately and manual detorsion attempted.
Torsion of the right testicle. The testicle lies horizontally
and in a higher position than the normal testicle.
The differential diagnosis of the acutely swollen or painful
scrotum also includes torsion of the testicular appendage, epididymitis,
orchitis, hernia, varicocele, tumor, trauma, idiopathic scrotal edema,
fat necrosis, viral inflammation, and Henoch-Schönlein
purpura.3,4As testicular torsion
is the diagnosis requiring the most urgent action, it should be
first on the differential diagnosis list. Testicular torsion
may result in irreversible damage to the involved testis. It may
also affect the contralateral testicle. Recent studies have examined
the possible immunologic mechanism for this global effect on fertility
but the exact pathophysiology has not been established.5,6
Testicular torsion results in the obstruction of the blood supply
to the testis. The venous obstruction leads to edema. This is followed
by arterial obstruction that leads to testicular ischemia. Because
the degree of torsion or vascular compromise cannot be quantified
by current methods, the time for torsion to result in irreversible
testicular damage cannot be determined.2 A complete vascular
occlusion will cause a testicle to develop permanent and irreversible
damage earlier than a testicle with partial vascular occlusion.
The literature is variable and cites a range of 6 to 24 hours of
vascular occlusion required to cause irreversible ischemic damage
to a testicle.7 Most authors agree that the best outcomes
are obtained with detorsion within 6 hours of symptom onset.
Testicular torsion may be classified as extravaginal or intravaginal.
Extravaginal torsion occurs primarily in neonates. The testis, epididymis,
and tunica vaginalis twist together on their vertical axis because
the gubernaculum has not yet become attached to the scrotal wall.
It is caused by the free rotation of the testicle around the spermatic
cord at a level above the tunica vaginalis. Intravaginal torsion
occurs in peri- or postpubertal males and has been associated with
the so-called bell-clapper deformity. In the normal scrotum, the
tunica vaginalis only partially covers the epididymis and does not
cover the spermatic cord. In the bell-clapper deformity, the tunica
vaginalis encases the entire testicle, epididymis, and base of the
spermatic cord. This allows the contents to twist and move within