A hydrocele is an accumulation of serous fluid in a body cavity. A hydrocele testis is the accumulation of fluids around a testicle. It is often caused by fluid collecting within a layer wrapped around the testicle, called the tunica vaginalis, which is derived from peritoneum. Provided there is no hernia present, it goes away without treatment in the first year. Although hydroceles usually develop in males, rare instances have been described in females.Primary hydroceles may develop in adulthood, particularly in the elderly and in hot countries, by slow accumulation of serous fluid. This is presumably caused by impaired reabsorption, which appears to be the explanation for most primary hydroceles, although the reason remains obscure. A hydrocele can also be the result of a plugged inguinal lymphatic system caused by repeated, chronic infection of Wuchereria bancrofti or Brugia malayi, two mosquito-borne parasites of Africa and Southeast Asia, respectively. As such, the condition would be a part of more diffuse sequelae commonly referred to as elephantiasis, which also affects the lymphatic system in other parts of the body. Presentation
Complications
Among the complications of hydrocele are:
Rupture usually occurs as a result of trauma but may be spontaneous. On rare occasions cure results after the fluid has been absorbed. Transformation into a haematocele occurs if there is spontaneous bleeding into the sac or as a result of trauma. Acute haemorrhage into the tunica vaginalis sometimes results from testicular trauma and it may be difficult without exploration to decide whether the testis has been ruptured.
Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherringtons Law describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherringtons Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally, there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction. Thus, tenth nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine-defective individuals are immune to motion sickness; why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherringtons Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.A recent theory  argues that the main reason motion sickness occurs is due to an imbalance in vestibular outputs favoring the semicircular canals (nauseogenic) vs. otolith organs (anti-nauseogenic). This theory attempts to integrate previous theories of motion sickness. For example, there are many sensory conflicts that are associated with motion sickness and many that are not, but those in which canal stimulation occurs in the absence of normal otolith function (e.g., in free fall) are the most provocative. The vestibular imbalance theory is also tied to the different roles of the otoliths and canals in autonomic arousal (otolith output more sympathetic). Diagnosis
The diagnosis is based on symptoms.