The physical examination of the scrotum may often be limited by pain, swelling, and skin changes [1]. It is important to carefully examine the skin of the scrotum, as there are both hair follicles and apocrine glands making it a frequent location for infection and sebaceous cysts. The testicles should be gently palpated between the fingertips using both hands. Under normal circumstances, the testicles should be firm and rubbery in consistency with a smooth surface. The epididymis is palpable as a ridge posterior to each testicle. In order to examine for a hernia, the clinician should place his or her index finger at the external inguinal ring by gently invaginating the scrotum. A hernia will be felt as a bulge when the patient is asked to bear down or valsalva. The valsalva maneuver will also make a varicocele more obvious on physical examination. Transillumination of the scrotum may be helpful in determining the difference between a solid mass or cystic mass [2].

In order to have a proper understanding of scrotal pain, one must first have a fundamental understanding of the anatomy and embryology of the scrotum and its contents. Understanding the origin of the testicle is very important as it helps to explain its vascular supply and innervation. For example, the close location of the developing kidneys and testes helps to explain why stones of the urinary tract can often present as testicular pain.

The developing testes are held loosely in place near the developing kidney by two ligamentous structures (the dorsal ligament or cranial suspensory ligament and the ventral ligament). Between 10 and 15 weeks gestation, the testes remains close to the inguinal region by enlargement of the gubernaculum and regression of the cranial suspensory ligament in the setting of enlargement of the abdominal cavity [3].

The layers covering the testicle starting from the outside include the skin, dartos fascia, external spermatic fascia, cremasteric fascia, cremasteric muscle, internal spermatic fascia, tunica vaginalis (parietal and then visceral), and lastly the tunica albuginea. The normal adult testis measures 4–5 cm in length, 3 cm in width, and 2.5 cm in depth with a volume of approximately 30 ml [4]. The right testicle usually lies anterior to the left [2].

The blood supply to the testicle is robust – there are three separate sources. The testicular artery (or gonadal artery) is the main blood supply to the testicle and arises directly from the aorta inferior to the superior mesenteric artery. Additional blood supply to the testicle comes from the cremasteric artery (branch of inferior epigastric) and the artery of the vas deferens (branch of the vesical arteries) [5].

The venous drainage of the testicle forms a pampiniform plexus that surrounds the testicular artery within the spermatic cord. Within the inguinal canal, these veins join to form larger veins and ultimately the gonadal vein in the abdomen. The gonadal vein on the right drains directly into the vena cava, while on the left it drains into the left renal vein [4].

The innervation of the testes arises from the aortic and renal plexus and travels along the course of the gonadal vessels [4]. Again this provides an explanation for referred pain patterns in obstructive ureteral stones. Nerves also arise from the pelvic plexus and travel next to the vas deferens. The relative anatomy of the nerves to recognizable structures is illustrated in Fig. 7.1. There may be cross-communication in these plexuses, explaining while testicular pain may be bilateral when there is only one diseased testis. The parietal and visceral tunica vaginalis and scrotal tissue are supplied by the genital branch of the genitofemoral nerve. However, its innervations stop at the tunica albuginea as the seminiferous tubules have no innervation [6].

Acute scrotal pain is potentially a medical emergency requiring necessitating a prompt evaluation to prevent potential testicular loss. The most common causes of acute scrotal pain include testicular torsion, torsion of the appendix testis, acute epididymitis, and testicular trauma. They will be discussed below.

Testicular torsion is defined as ischemia of the testicle secondary to rotation of the testicle along its longitudinal axis. There is a short window of approximately 4–8 h from the start of torsion symptoms until surgical intervention is required to save the affected testicle [7].

The prevalence of testicular torsion in men aged 1–25 years in the United States has been estimated from a nationwide inpatient sample to be 4.5 cases per 100,000 male patients per year [7]. The age distribution of testicular torsion has is bimodal, with an increased frequency in the first year of life and in early adolescence. In a cohort analysis of 2443 patients ages 1 to less than 18, testicular loss was seen in 42 % of the boys undergoing surgery for testicular torsion. Age less than 10 is associated with increased rate of loss [8].

Extravaginal torsion, defined as twisting of the entire cord and processus vaginalis, is more common in the neonatal period. Intravaginal torsion, defined as twisting of the cord within the tunica vaginalis, is seen in early adolescence. It has a higher incidence and is seen with the bell-clapper deformity, a condition in which the testicle has more mobility within the tunica vaginalis [9, 10]. The majority of testicular torsion occurs in a medial direction and clinicians can attempt de-torsion by turning the testicle in the same way they turn the pages of a book. However, several studies have shown torsion in the lateral direction in up to 29–33 % of cases [11, 12].

Testicular torsion often has a classic presentation of sudden onset severe unilateral scrotal pain. Pain that persists after the administration of opioid analgesia makes the suspicion for torsion higher. The patient may report previous bouts of intermittent pain likely secondary to episodes of torsion and spontaneous detorsion. The presences of reflexive nausea and emesis can also be seen in up to 57–69 % of patients. On physical examination, the affected testicle is usually high riding and extremely tender. Venous distention and transudate often cause the affected testicle to be large in size compared to the contralateral testicle. Loss of the cremasteric reflex is also an important finding that increases suspicion for torsion [11].

Patients who have a history and physical exam strongly concerning for testicular torsion should be referred immediately for surgical exploration. Surgical exploration should not be delayed to obtain imaging as each minute of extending ischemia can decrease testicular survival rates [9]. The testicle can usually be saved 90 % of the time if de-torsion is performed within 6 h. After 12 h 50 % of testicles are viable. After 24 h less than 10 % are viable [13]. Doppler ultrasound is the most commonly used to evaluate the acute scrotum and has been found to be highly sensitive (88.9 %) and specific (98.8 %) for testicular torsion with a 1 % false-negative rate [14].

During testicular exploration, the testicle should be detorsed as quickly as possible and bilateral orchiopexy should be performed with permanent suture. The contralateral testicle is pexied regardless of the viability of the affected testicle [15] because the bell-clapper deformity is bilateral in up to 80 % of patients [16].

The urgency of diagnosis and treatment and a relatively high rate of adverse outcomes make testicular torsion a common area of litigation. The urologist usually suffers the bulk of the litigation burden. The most common liability seen in litigation is a missed diagnosis. The urologist does not need to practice defensive medicine. However, he or she should strongly consider exploring the scrotum when the diagnosis is in question. Furthermore, based on previous litigation data, a prophylactic contralateral orchiopexy should always be performed when torsion is found [17].

The testicular appendage is a remnant of the Mullerian duct, whereas epididymal appendages are from the mesonephric or Wolffian duct [18]. In a retrospective study of 138 patients with acute scrotal symptoms, 67 % of patients had torsion of an appendix testis [19]. Torsion of an appendage occurs more frequently in the prepubertal age group likely because increased hormonal stimulation enlarges the appendages, making them more susceptible to twisting. The presentation of a patient with torsion of an appendix testis usually has a sudden onset of pain similar to testicular torsion [18]. However, the occurrence of nausea and vomiting is usually less frequent [19].

Early after the onset of torsion on physical exam, the inflamed and ischemic appendage can be seen through the skin and is known as the “blue-dot sign.” However, as local inflammation occurs the surrounding tissues become edematous and the diagnosis is not always clear. The use of a scrotal ultrasound after the inflammation has occurred often observes increased blood flow to the adjacent epididymis and testis and possibly a reactive hydrocele. These findings often cause many clinicians to come to the incorrect diagnosis of acute epididymitis or epididymo-orchitis. Fortunately, torsion of the appendix testis is self-limited and surgical intervention is not necessary. As the appendage infarcts the pain dissipates. Nonsteroidal anti-inflammatory medications (NSAIDS) are the mainstay of treatment in addition to comfort measures such as limited activity and warm compresses. A patient can present with torsion of an appendage more than once; there are potentially five anatomic sites where appendages may exist and more than one appendage may occur in a given site [18].

Epididymitis is extremely common and usually secondary to retrograde ascent of an infectious pathogen. It has been reported to account for 0.3–0.69 % of outpatient visits [20, 21]. In men between the ages of 14 and 35, the most common infectious organisms are Neisseria gonorrhoeae and Chlamydia trachomatis. In patients younger than 14 or older than 35, epididymitis is usually caused by common urinary tract pathogens [21]. In about 30–40 % of patients, the etiology of the epididymitis cannot be found [20].

The presentation of epididymitis is usually gradual onset of pain. If caused by urinary tract pathogens, lower urinary tract symptoms, such as frequency urgency, hematuria, and dysuria, may be present. Having such lower urinary tract symptoms would be rare in testicular torsion. Nausea and vomiting is not common and can help differentiate between epididymitis and testicular torsion [21]. Acute-phase proteins, such as C-reactive protein (CRP), have also been used to help differentiate between epididymitis and testicular torsion. A significant elevation in CRP had a 96.2 sensitivity and 94.25 specificity in a study of 104 patients with an acute scrotum [22]. On ultrasound examination, one usually finds an enlarged epididymitis with increased Doppler flow. In one study on children, color Doppler ultrasound was shown to have a 70 % sensitivity and 88 % specificity for epididymitis [23]. However, in cases where there are any doubts about the diagnosis operative exploration should be performed.

Isolated inflammation of the testicle is relatively uncommon; however, it can be seen with viruses such as mumps and coxsackie or bacteria, such as Mycobacterium tuberculosis, Treponema pallidum and Brucella spp [28]. Viral orchitis is usually associated with an abrupt onset of unilateral pain. Mumps orchitis is a common cause of viral and occurs in 20–30 % of males with a mumps infection [21]. With a mumps infection, the orchitis usually develops 4–7 days after the development of parotitis [20, 21].

Scrotal trauma can occur commonly during sports, motor vehicle accidents, assaults, and straddle injuries. Testicular rupture requires urgent surgical exploration. Additionally, if a scrotal hematoma is large enough exploration should be strongly considered [24]. Avulsion injuries of the scrotum can usually be closed even with large tissue loss. All penetrating injuries that violate the dartos fascia should be explored [25]. In cases of children with scrotal trauma, sexual abuse should be considered.

Given the large amount of hair follicles and apocrine glands on the scrotum infections of the scrotal wall are not uncommon. Fournier gangrene or necrotizing fasciitis involving the genital area is rare but has high lethal potential. Diabetes, alcoholism, urethral stricture disease, and immunosuppression place individuals at higher risk. Local trauma, urine extravasation, paraphimosis, perianal infections, and surgery in the region can be inciting factors. Early symptoms are similar to cellulitis; however, Fournier’s gangrene progresses rapidly and causes swelling, crepitus, discoloration, and necrosis of the skin and soft tissue. Prompt diagnosis, emergent antibiotics and surgical debridement is essential [26].

Other notable causes of acute scrotal pain include inguinal hernias, acute idiopathic scrotal edema, testicular cancer, varicocele, hydrocele, Henoch–Schonlein purpura, and referred pain.