Hydrocele

Embryological basis

The processus vaginalis begins as a protrusion of the peritoneum around the 12^th week of gestation and extends into the scrotum in boys. The scrotal part of the processus vaginalis mostly surrounds the testis to form the tunica vaginalis, although the posterior aspect of the testis that is attached to the epididymis is not covered by the tunica. Following testicular descent, the proximal aspect of the processus undergoes obliteration.

The corresponding s​tructure in females extends in the canal of Nuck and is attached to the ipsilateral labia. ^[3] (See the image below.)

Hydroceles have been classified as primary or secondary. Primary hydroceles are those of congenital origin and may be further divided into communicating or non-communicating (ie, with or without patency between peritoneum and scrotum). Secondary hydroceles are caused by conditions such as inflammation, infection, previous surgeries, or testicular torsion.

The presence of a hydrocele alone has minimal clinical significance. Hydroceles do not have an effect on later fertility. The primary concern is to rule out associated malignancy, infection, or other treatable conditions. Symptoms, primarily size and discomfort, are typically the reasons that patients seek medical attention.  

A patent processus vaginalis is found in 80-90% of term male infants at birth. This frequency rate steadily decreases until age 2 years, at which point it appears to plateau at approximately 25-40%. Despite this, hydroceles are only observed in 1-5% of children. ^[4] Transforming growth factor beta1 (TGFβ1), which is a potent fibrogenic agent, may stimulate fibrosis and closure of the processus vaginalis. ^[5] Certain conditions, such as breech presentation, prematurity, ^[4] gestational progestin use, and low birth weight, have been associated with an increased risk of hydroceles.

In a Swedish study, the annual incidence of hydroceles in patients age 18 years and older who presented to specialized healthcare was 60 per 100,000 men. However, surgical management of hydrocele or spermatocele was required in only 17 per 100,000 men. ^[6]

Worldwide, the most common cause of hydrocele in the adult population is filariasis, a parasitic infestation caused by Wuchereria bancrofti (see Filarial Hydrocele). Filariasis affects more than 90 million people in more than 52 countries. ^[7] However, this condition is virtually nonexistent in the United States.

The World Health Organization (WHO) considers lymphatic filariasis (LF) to be endemic in 72 countries, including Brazil, the Dominican Republic, Guyana, and Haiti in the Americas. Rates of hydrocele in endemic areas can reach 25% in males with LF. ^[8]

In children, most hydroceles are congenital and of the communicating type, in which patency of the processus vaginalis allows peritoneal fluid to flow into the scrotum, particularly during Valsalva maneuvers. With noncommunicating hydroceles, in both children and adults, fluid accumulates because of altered balance between fluid production and absorption within the tunica. Noncommunicating hydroceles can also be congenital, or they may result from conditions such as inflammation, infection, previous surgeries, or testicular torsion. ^[3]

Following laparoscopic or transplant surgery in males, inadequate aspiration of irrigation fluid may cause hydroceles in patients with a patent processus vaginalis or a small hernia. Careful aspiration of fluid at the end of laparoscopic procedures helps prevent this complication.

A few studies have attempted to show a link between certain molecular derangements and an increased incidence of patent processus vaginales (and therefore hydroceles and indirect hernias). Two such examples include increases in maternal estrogen concentrations during pregnancy and abnormalities in the calcitonin gene–related peptide (CGRP) released by the genitofemoral nerve. ^[9]

Mesotheliomas of the tunica vaginalis are rare, but should be considered in patients with a history of asbestos exposure who have a complex hydrocele with hypervascular parietal vegetations. ^{[10, 11, 12]}

Filariasis, a parasitic infestation caused by Wuchereria bancrofti, accounts for most causes of hydroceles in adults worldwide, affecting more than 90 million people in more than 52 countries. ^[7] However, this condition is virtually nonexistent in the United States, where iatrogenic causes of hydroceles predominate.

The pathophysiology of hydroceles involves an imbalance between scrotal fluid production and absorption. This imbalance can be divided further into exogenous fluid sources or intrinsic fluid production.

A commonly utilized classification system classifies hydroceles into primary, secondary communicating, secondary non-communicating, microbe-induced, inflammatory, iatrogenic, trauma induced, tumor induced, canal of Nuck or giant. ^[13] This classification is based on the possible etiology but can be confusing to utilize. Hoang et al have proposed an updated classification system that divides primary hydrocele into the following 7 types, on the basis of findings at surgery ^[14] :

1. Peritesticular or vaginal hydrocele; if fluid is excessive, leads to abdominoscrotal hydrocele
2. Noncommunicating hydrocele without hernia
3. Noncommunicating hydrocele with hernia
4. Communicating hydrocele without hernia
5. Communicating hydrocele with hernia
6. Noncommunicating hydrocele of the spermatic cord and the scrotum; if fluid is excessive, leads to abdominoscrotal hydrocele
7. Encysted spermatic cord hydrocele, or encysted hydrocele of the canal of Nuck

In general, most urologists limit classification to communicating or non-communicating, as this has a direct impact on the surgical management. Abdominoscrotal hydroceles can be considered in a separate category, and most likely are similar to canal of Nuck hydroceles.

Communicating hydroceles

Communicating hydroceles are typically noted in children and are associated with a persistent patent processus vaginalis (PPV). In a prospective study of 526 infants younger than 4 months who were undergoing laparoscopic pyloromyotomy, PPV was noted in 54%; however, when followed for > 1 year, only 1.2% of those patients required surgical management for the PPV. ^[15]

Management tends to be expectant during the first year of life. For PPV that persists beyond the first year of life, or causes symptoms, surgical care may be recommended.

Communicating hydroceles may also be due to iatrogenic causes, such as migration of a ventriculoperitoneal shunt or extension of peritoneal fluid from intraperitoneal dialysis.  

Open or laparoscopic techniques for treatment of hydrocele have similar outcomes. There is a 15% incidence of PPV in the contralateral inguinal region, when evaluated at the time of surgery. ^[16] Management of communicating hydroceles requires approaching the PPV in the inguinal canal rather than through the scrotum.

Noncommunicating hydroceles

Noncommunicating hydroceles may result from increased fluid production or impaired fluid absorption. Multiple causes have been cited for the development of noncommunicating hydroceles. This is typically the type of hydrocele noted in patients with filariasis. Noncommunicating hydroceles may also be secondary to torsion of the appendix testis, tumors, or inflammatory or infectious conditions, including syphilis, tuberculosis, and epididymitis.

Other potential iatrogenic causes include varicocele surgery that leads to disruption of the lymphatic system. In patients with a penile prosthesis, secondary hydrocele due to migration of the pump has been reported.

Abdominoscrotal hydroceles

This is the most uncommon type of hydrocele. These have an inguinoscrotal component, with a second larger or small intra-abdominal component. The intra-abdominal component can be so large that it can cause renal obstruction. ^[17]

Hydroceles typically manifest as a soft nontender fullness within the hemiscrotum that occur over a variable period of time. If communicating, the hydrocele will increase in size with increased intra-abdominal pressure and decrease in size when the patient is lying supine. ^[4] The testis is generally palpable along the posterior aspect of the fluid collection. When the scrotum is investigated with a focused beam of light, the scrotum transilluminates, revealing a homogeneous glow without internal shadows.

Hydroceles of the canal of Nuck in female patients typically present as soft, nontender inguinal or labial swelling. See the image below. Like hemiscrotal hydroceles, labial hydroceles transilluminate readily. ^{[18, 19]}

Indications for intervention in hydroceles include the following:

• Inability to distinguish from an inguinal hernia
• Failure of the hydrocele to resolve spontaneously after an appropriate interval of observation
• Inability to clearly examine testis
• Association of hydroceles with suggestive pathology (eg, torsion, tumor)
• Pain or discomfort
• Male infertility
• Cosmesis

The developmental anatomy of the inguinal canal is responsible for the genesis of pediatric communicating hydroceles. As the testis descends from the posterolateral genitourinary ridge at the beginning of the third trimester of fetal gestation, a saclike extension of peritoneum descends in concert with the testis. As descent progresses, the sac envelops the testis and epididymis. The result is a serosal-lined tubular communication between the abdomen and the tunica vaginalis of the scrotum.

The peritoneum-derived serosal communication is the processus vaginalis, and the serosa of the hemiscrotum becomes the tunica vaginalis. At term, or within the first 1-2 years of life, the processus vaginalis of the spermatic cords fuse, thereby obliterating the communication between the abdomen and the scrotum. The processus fuses distally as far as the lower epididymal pole and anteriorly to the upper epididymal pole. Failure of complete fusion may result in communicating hydroceles, indirect inguinal hernias, and the bell-clapper deformity of abnormal testicular fixation in the scrotum. ^[20]

No true absolute contraindications exist for repair of hydroceles. However, given the minimal clinical consequence of the hydrocele itself, any condition that classifies patients as poor surgical or anesthetic risk may be considered a relative contraindication to surgical repair.

Additionally, while a slight majority of pediatric surgeons across North America would repair any communicating hydrocele (somewhat irrespective of age) if it were clearly communicating, waiting until the child is 1-2 years old is certainly reasonable. Finally, small atrophic testes, or solitary testes, should be approached with great caution to minimize the risk of anorchia.

In a review of data from 355 pediatric patients with hydroceles, Acer-Demir et al reported high rates of spontaneous resolution, with virtually all children older than 1 year of age who did not undergo surgery showing spontaneous resolution within 1 year. ^[21] These authors recommend monitoring congenital hydroceles until at least 1 year and preferably 2 years of age, unless strong evidence of hydrocele-induced testicular damage arises, and recommend monitoring noncongenital hydroceles for at least 6 months and preferably 1 year if the patient has no associated pathology indicating the need for earlier surgery. ^[21]