Teaching Case

A 72-year-old male patient presented to our Emergency Department with discomfort and pain in the left scrotum for 13 days. He underwent surgery for left inguinal hernia (Lichtenstein technique) 13 days before. There was a history of another surgery for inguinal hernia in the same location many years ago.

Ultrasound examination revealed left testicle diffusely hypoechoic with absent flow Doppler. There was increased vascularity in the periphery of the left scrotum. These findings are compatible with testicular ischaemia secondary to hernioplasty.
The right testicle was of normal size and morphology with colour Doppler flow was without identifying focal lesions. Mild bilateral hydrocele.

Testicular ischaemia is a rare complication of inguinal hernia repair.
Internal spermatic arteries originate from the aorta just inferior to the renal arteries. They course through the deep inguinal ring to enter the spermatic cord. The testicular artery penetrates the tunica albuginea along the posterior aspect of the testis and gives off capsular branches which course through the tunica vasculosa.
Supply to the epididymis and other extratesticular structures comes from the deferential artery (arises from the internal iliac artery) and the cremasteric artery (arises from the inferior epigastric artery). They join the spermatic cord at the inguinal ring [1]
The main testicular complications of inguinal hernia surgery are ischaemic orchitis and testicular atrophy [2]. The risk is greater after repair by an anterior approach and recurrent hernias.
Orchitis usually manifest 24-72 hours after surgery, with enlarged testicles, painful on palpation and hard consistency. The intensity and duration of clinical varies. Testicular pain usually lasts for weeks, while induration and enlargement may persist longer. In rare occasions testicular necrosis requiring orchiectomy may develop.
Many factors should join in testicular ischaemia such as the disruption of the internal spermatic artery, an excessive closing of the internal and external inguinal rings causing thrombosis of the veins and mobilization of the testicle out of the scrotum that compromises the collateral circulation [2].
The natural course of testicular ischaemia without treating the cause is testicular atrophy.
The diagnosis of testicular ischaemia is confirmed by colour Doppler ultrasound when there is no detectable flow in the testicular parenchyma. In subacute or chronic phases it is possible to visualize peritesticular hyperaemia [3, 4].

In this case the patient had a history of 13 days of pain in the left scrotum with ultrasound findings of testicular ischaemia. His surgeon decided on conservative treatment.

In the differential diagnosis we included spermatic cord torsion, which is the most common cause of testis ischaemia. Torsion can occur at any age but is most common in adolescent males. Ultrasound findings depend on the time of evolution, the testicle may be normal or hypoechoic on greyscale imaging. Colour Doppler ultrasound shows an absence of flow in the symptomatic testicle [5].

Contrast enhanced ultrasound (CEUS) is increasingly used for non-hepatic applications, like some pathologies in the testis. CEUS is extremely effective in assessing presence or lack of organ perfusion and could be used in cases where conventional Doppler ultrasound fails to detect flow [6].