A ureterovaginal fistula is an abnormal passageway existing between the ureter and the vagina. It presents as urinary incontinence. Its impact on  women is to reduce the "quality of life dramatically." Cause
A ureterovaginal fistula is a result of trauma, infection, pelvic surgery, radiation treatment and therapy, malignancy, or inflammatory bowel disease. Symptoms can be troubling for women especially since some  clinicians delay treatment until inflammation is reduced and stronger tissue has formed. The fistula may develop as a maternal birth injury from a long and protracted labor, long dilation time and expulsion period. Difficult deliveries can create pressure necrosis in the tissue that is being pushed between the head of the infant and the softer tissues of the vagina, ureters, and bladder.Radiographic imaging can assist clinicians in identifying the abnormality. A Ureterovaginal fistula is always indicative of an obstructed kidney necessitating emergency intervention followed later by an elective surgical repair of the fistula. Treatment
Many women delay treatment for decades. Surgeons often will correct the fistula through major gynecological surgery. Newer treatments can include the placement of a stent and is usually successful. In 0.5-2.5% of major pelvic surgeries a ureterovaginal fistula will form, usually weeks later. If the fistula cannot be repaired, the clinician may create a permanent diversion of urine or urostomy. Risks associated with the repair of the fistula are also associated with most other surgical procedures and include the risk of adhesions, disorders of wound healing, infection, ileus, and immobilization.
The phonatory muscles are divided into adductors (lateral cricoarytenoid muscles, arytenoid muscles) and tensors (cricothyroid muscles, thyroarytenoid muscles). Intrinsic
The intrinsic laryngeal muscles are responsible for controlling sound production. Cricothyroid muscle lengthen and tense the vocal cords. Posterior cricoarytenoid muscles abduct and externally rotate the arytenoid cartilages, resulting in abducted vocal cords. Lateral cricoarytenoid muscles adduct and internally rotate the arytenoid cartilages, increase medial compression. Transverse arytenoid muscle adduct the arytenoid cartilages, resulting in adducted vocal cords. Oblique arytenoid muscles narrow the laryngeal inlet by constricting the distance between the arytenoid cartilages. Thyroarytenoid muscles narrow the laryngeal inlet, shortening the vocal cords, and lowering voice pitch. The internal thyroarytenoid is the portion of the thyroarytenoid that vibrates to produce sound.Notably the only muscle capable of separating the vocal cords for normal breathing is the posterior cricoarytenoid. If this muscle is incapacitated on both sides, the inability to pull the vocal cords apart (abduct) will cause difficulty breathing. Bilateral injury to the recurrent laryngeal nerve would cause this condition. It is also worth noting that all muscles are innervated by the recurrent laryngeal branch of the vagus except the cricothyroid muscle, which is innervated by the external laryngeal branch of the superior laryngeal nerve (a branch of the vagus). Additionally, intrinsic laryngeal muscles present a constitutive Ca2+-buffering profile that predicts their better ability to handle calcium changes in comparison to other muscles. This profile is in agreement with their function as very fast muscles with a well-developed capacity for prolonged work.