Diagnosis
There are various ways of diagnosing this congenital heart defect both prenatally and postnatally, these methods include:
Ultrasound
Pulse oximetry
Chest X-ray
Echocardiogram
Electrocardiogram
Cardiac catheterization
Cardiac CT scan
Genetic testing (particularly if other systemic birth anomalies are seen alongside the pulmonary atresia and ventricular septal defect). Management
When the disorder is detected (usually before or soon after birth), prostaglandin will be temporarily used as soon as possible in order to keep the ductus arteriosus open for as long as possible until surgery can be done, this is done so that blood can keep flowing to the lungs, since the bodies of babies with pulmonary atresia usually use the ductus arteriosus for lung blood flow pre-natally until birth, after which it closes.Afterwards, this anomaly is usually managed with surgeries for improvement of blood flow and function of the heart, although what kind of treatment one gets depends on the structure of the cardiorespiratory system.The surgical methods that can be used to treat (for the long-term) this condition include:
Catheter procedure for pulmonary artery branches
Systemic-to-pulmonary artery shunt
Neonatal complete repair
One-stage complete repair
Balloon septostomy

Staged unifocalization

Frequency
Frequency estimates vary between populations, estimates range from 0.01% to 0.2% of live births with PAVSD. It is believed to make up for 1-2% of cases of congenital heart defects worldwide.Of all patients with PAVSD, around 25-32% of them have a microdeletion of the 22q11.2 chromosome. Prognosis
Without treatment, it is a highly life-threatening condition, so prognosis is poor.
Similarly, the degree to which transthyretin amyloidosis-associated polyneuropathy and carpal tunnel syndrome is under investigation. Prior carpal tunnel release is often noted in individuals who later present with transthyretin amyloid-associated cardiomyopathy. There is consideration that bilateral carpal tunnel syndrome could be a reason to consider amyloidosis, timely diagnosis of which could improve heart health. Amyloidosis is rare, even among people with carpal tunnel syndrome (0.55% incidence within 10 years of carpal tunnel release). In the absence of other factors associated with a notable probability of amyloidosis, its not clear that biopsy at the time of carpal tunnel release has a suitable balance between potential harms and potential benefits.Other specific pathophysiologies that can cause median neuropathy via pressure include:

Rheumatoid arthritis and other diseases that cause inflammation of the flexor tendons. With severe untreated hypothyroidism, generalized myxedema causes deposition of mucopolysaccharides within both the perineurium of the median nerve, as well as the tendons passing through the carpal tunnel. Association of CTS and IMNCT with lesser degrees of hypothyroidism is questioned. Pregnancy may bring out symptoms in genetically predisposed individuals. Perhaps the changes in hormones and fluid increase pressure temporarily in the carpal tunnel. High progesterone levels and water retention may increase the size of  the synovium. Bleeding and swelling from a fracture or dislocation. This is referred to as acute carpal tunnel syndrome. Acromegaly causes excessive secretion of growth hormones.