Potassium is not in fact lost from the body, but increased Na+/K+-ATPase activity (the enzyme that moves potassium into cells and keeps sodium in the blood) leads to shift of potassium into tissues, and depletes the circulation. In other types of potassium derangement, the acid-base balance is usually disturbed, with metabolic alkalosis and metabolic acidosis often being present. In TPP, these disturbances are generally absent. Hypokalemia leads to hyperpolarization of muscle cells, making the neuromuscular junction less responsive to normal nerve impulses and leading to decreased contractility of the muscles.It is not clear how the described genetic defects increase the Na+/K+-ATPase activity, but it is suspected that the enzyme becomes more active due to increased thyroid hormone levels. Hyperthyroidism increases the levels of catecholamines (such as adrenaline) in the blood, increasing Na+/K+-ATPase activity. The enzyme activity is then increased further by the precipitating causes. For instance, increased carbohydrate intake leads to increased insulin levels; this is known to activate Na+/K+-ATPase. Once the precipitant is removed, the enzyme activity returns to normal levels. It has been postulated that male hormones increase Na+/K+-ATPase activity, and that this explains why males are at a higher risk of TPP despite thyroid disease being more common in females.TPP is regarded as a model for related conditions, known as "channelopathies", which have been linked with mutations in ion channels; the majority of these conditions occurs episodically. Diagnosis
Hypokalemia (low blood potassium levels) commonly occurs during attacks; levels below 3.0 mmol/L are typically encountered. Magnesium and phosphate levels are often found to be decreased.
The possible mechanisms by which vesicouterine fistulas occur following caesarean sections include undetected bladder injury during caesarean section, inadvertent placement of a suture through the bladder during the repair of the uterus and abnormal blood vessel connections following multiple caesarean sections.It may also present following use of obstetric forceps, manual placenta removal, external cephalic version, morbidly adherent placenta, surgical removal of fibroids, rupture of the uterus, perforation of the uterus and radiation therapy in the treatment of cervical cancer.Vesicouterine fistula can also occur as a birth defect in conjunction with vaginal atresia. Diagnosis
The diagnosis of a vesicouterine fistula is made by demonstrating an abnormal connection between the cavities of the bladder and uterus. It can be diagnosed using hysterosalpingography, hysterography, cystography, magnetic resonance imaging (MRI) and computerised tomography. MRI has been found to have 100% accuracy in the diagnosis of vesicouterine fistula. It is also less invasive than other modalities and is considered the gold standard for diagnosis. Treatment
The options of treatment include watchful waiting for spontaneous resolution of the fistula, use of medications that can stop menstrual periods such as oral contraceptive pills, progesterone and gonadotropin releasing hormone analogs. Surgery can be carried out through the vagina, bladder or peritoneum and can be done via laparoscopic or robotic surgery.Watchful waiting is the treatment of choice in case of small fistulas. The bladder is catheterised for a period of 4 to 8 weeks in order to allow spontaneous closure of the vesicouterine fistula.