Hydrocele

The description of the abdominal cavity parietes to the tunica vaginales is attributed to Galen in 176 AD. However, the clear description of the inguinal anatomy and its relationship to groin hernias and hydroceles was not recorded until the 19th century.

The presence of fluid within the hemiscrotum has little clinical impact on the testis. However, determining the cause for the increased fluid, specifically any associated clinically significant pathology, remains the primary concern with regard to hydroceles. Once pathology that is more ominous has been excluded, persistence of the hydrocele or associated discomfort may indicate the need for surgical intervention.

Patients who have undergone varicocelectomy may be an important exception in which a hydrocele may be of clinical importance. This procedure is usually performed when dilated vessels around the testes are believed to increase intratesticular temperatures, thereby leading or contributing to male infertility. Varicocelectomy may damage nearby lymphatic vessels, which may lead to the formation of postvaricocelectomy hydroceles in approximately 7% of patients, potentiating the insulation of the testicle and leading to persistent problems with sperm production. The use of microscopes during this procedure has significantly decreased the incidence of lymphatic obliteration and, therefore, hydrocele formation.

Frequency

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%. Indeed, autopsy series of men have identified a frequency rate of 20% of the processus vaginalis remaining patent until late in life. However, clinically apparent scrotal hydroceles are evident in only 6% of term males beyond the newborn period. Certain conditions, such as breech presentation, gestational progestin use, and low birth weight, have been associated with an increased risk of hydroceles. The incidence of hydroceles in men is less well known. See the image below.

Hydrocele. Small patent processus vaginalis (indicated by the bubbles) as viewed laparoscopically.

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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. ^[6]

The causes of hydroceles are legion. In children, most hydroceles are of the communicating type, in which patency of the processus vaginalis allows peritoneal fluid to flow into the scrotum, particularly during Valsalva maneuvers.

In the adult population, filariasis, a parasitic infection caused by Wuchereria bancrofti, accounts for most causes of hydroceles worldwide, affecting more than 90 million people in more than 52 countries. ^[7] (see Hydrocele, Filarial) However, this condition is virtually nonexistent in the United States, where iatrogenic causes of hydroceles predominate.

Following laparoscopic or transplant surgery in males, inadequate irrigation fluid aspiration 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. In noncommunicating hydroceles, for both children and adults, the balance between fluid production within the tunica and the fluid absorption is altered.

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. ^[8]

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. ^{[9, 10, 11]}

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

Alternatively, hydroceles can be divided into those that represent a persistent communication with the abdominal cavity and those that do not. Fluid excesses are from exogenous sources (the abdomen) in communicating hydroceles, whereas noncommunicating hydroceles develop increased scrotal fluid from abnormal intrinsic scrotal fluid shifts.

Communicating hydroceles

With communicating hydroceles, simple Valsalva maneuvers probably account for the classic variation in size during day-sleep cycles. Nonetheless, with the incidence of patent processus so great, why children with clinically apparent hydroceles are relatively few remains somewhat inexplicable. Chronically increased intra-abdominal pressure (eg, as in chronic lung disease) or increased abdominal fluid production (eg, children with ventriculoperitoneal shunts) probably warrants early surgical intervention.

Noncommunicating hydroceles

Noncommunicating hydroceles may result from increased fluid production or impaired fluid absorption. A sudden onset of scrotal hydrocele in older children has been noted after viral illnesses. In such cases, viral-mediated serositis may account for the net increased fluid production. Posttraumatic hydroceles likely occur secondary to increased serosal fluid production due to underlying inflammation. Although rare in the United States, filarial infestations are a classic cause of the decreased lymphatic fluid absorption resulting in hydroceles.

Hydroceles typically manifest as a soft nontender fullness within the hemiscrotum. 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. Like hemiscrotal hydroceles, labial hydroceles transilluminate readily. ^{[3, 4]}

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. ^[1]

Seemingly, 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 recovery within 1 year. 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. ^[12]