Treatment depends on the anatomy of the malformation as determined by angiography or Magnetic Resonance Imaging (MRI).

Testing for a malformed vein of Galen is indicated when a patient has heart failure which has no obvious cause. Diagnosis is generally achieved by signs such as cranial bruits and symptoms such as expanded facial veins. The vein of Galen can be visualized using ultrasound or Doppler. A malformed Great Cerebral Vein will be noticeably enlarged. Ultrasound is a particularly useful tool for vein of Galen malformations because so many cases occur in infancy and ultrasound can make diagnoses prenatally. Many cases are diagnosed only during autopsy as congestive heart failure occurs very early.

Symptoms of congenital PSS usually appear by six months of age and include failure to gain weight, vomiting, and signs of hepatic encephalopathy (a condition where toxins normally removed by the liver accumulate in the blood and impair the function of brain cells) such as seizures, depression, tremors, drooling, and head pressing. Urate bladder stones may form because of increased amounts of uric acid in circulation and excreted by the kidneys. Initial diagnosis of PSS is through laboratory bloodwork showing either elevated serum bile acids after eating or elevation of fasting blood ammonia levels, which has been shown to have a higher sensitivity and specificity than the bile acids test.

Various diagnostic imaging techniques are used to demonstrate PSS. Ultrasonography is a rapid, convenient, non-invasive, and accurate method for diagnosis of PSS. Ultrasonographic diagnosis of congenital PSS depends on finding an anomalous vessel either in the liver or just caudal to the liver in the dorsal abdomen, usually draining into the caudal vena cava. Ultrasonography can also be used to estimate hepatic volume and vascularity, and to identify related lesions affecting other abdominal structures, such as urinary calculi. Computed tomography (CT) may be considered when ultrasound expertise is lacking or ultrasonography is considered sub-optimal (e.g. because of the conformation of the patient). Control of respiration and careful timing of CT acquisition after contrast injection is necessary for optimal depiction of PSS. Rectal portal scintigraphy using technetium pertechnetate, a technique of imaging involving detection of gamma rays emitted by radionuclides absorbed through the rectum and into the bloodstream, demonstrates the blood vessel bypassing the liver. In certain institutions, scintigraphy is the preferred diagnostic technique, but this leaves the patient radioactive for 24h, which may be inconvenient depending on nursing needs. Portal venography is the definitive method for demonstrating PSS, but is invasive, hence it is best reserved for animals with a known shunt or those considered highly likely to have a shunt that was not detectable by ultrasonography.

Hypoplastic right heart syndrome is less common than hypoplastic left heart syndrome which occurs in 4 out of every 10,000 births. [3].

This rare anomaly requires prenatal diagnosis since it needs immediate and emergency treatment. Pregnant women whose pregnancy is complicated with this anomaly should be referred to a level 3 hospital with pediatric cardiology and pediatric cardiothoracic surgical team.[3]

It can be associated with aortic stenosis.

The surgical treatment involves the resection of the extracranial venous package and ligation of the emissary communicating vein. In some cases of SP, surgical excision is performed for cosmetic reasons. The endovascular technique has been described by transvenous approach combined with direct puncture and the recently endovascular embolization with Onyx.

With a series of operations or even a heart transplant, a newborn can be treated but not be cured. Young individuals who have undergone reconstructive surgery must refer to a cardiologist who is experienced in congenital heart diseases, "Children with HLHS are at an increased level for developing endocarditis." Kids that have been diagnosed with HRHS must limit the physical activity they participate in to their own endurance level.

These lesions usually present in neonates, although they may not come to clinical attention until adulthood (for cosmetic reasons). There is no gender predilection. They are present in approximately 3-6 per 1000 live births.

Simple surgical excision is curative. The recommended treatment is that the skin is peeled off the extra-auricular tissue and protruding cartilage remnants are trimmed. Normal appearance is achieved in majority of cases. The reconstruction successful in true cases of accessory auricle, as it also is in individuals with auricular appendages.

Occasionally, there is only the one single umbilical artery (SUA) present in the umbilical cord. Approximately this affects between 1 in 100 and 1 in 500 pregnancies, making it the most common umbilical abnormality. It is more common in multiple births. Its cause is not known.

Most cords have one vein and two arteries. The vein carries oxygenated blood from the placenta to the baby and the arteries carry deoxygenated blood from the baby to the placenta. In approximately 1% of pregnancies there are only two vessels —usually a single vein and single artery. In about 75% of those cases, the baby is entirely normal and healthy and the missing artery isn't missed at all. One artery can support a pregnancy and does not necessarily indicate problems. For the other 25%, a 2-vessel cord is a sign that the baby has other abnormalities—sometimes life-threatening and sometimes not. SUA does increase the risk of the baby having cardiac, skeletal, intestinal or renal problems. Babies with SUA may have a higher likelihood of having other congenital abnormalities, especially of the heart. However, additional testing (high level ultrasound scans) can rule out many of these abnormalities prior to birth and alleviate parental anxiety. Echocardiograms of the fetus may be advised to ensure the heart is functioning properly. Genetic counseling may be useful, too, especially when weighing the pros and cons of more invasive procedures such as chorionic villus sampling and amniocentesis.

Although the presence of an SUA is a risk factor for additional complications, most fetuses with the condition will not experience other problems, either in utero or after birth. Especially encouraging are cases in which no other soft markers for congenital abnormalities are visible via ultrasound. Prior to ultrasound technology, the only method for determining the presence of a SUA was at birth, following an examination of the placenta. Given that the vast majority of expectant mothers do not receive the kind of advanced ultrasound scanning required to confirm SUA in utero, most cases may never be detected antenatally even today.

Doctors and midwives often suggest parents take the added precaution of having regular growth scans near term to rule out intrauterine growth restriction, which can happen on occasion and warrant intervention. Yet the majority of growth restricted infants with the abnormality also have other defects. Finally, neonates with the finding may also have a higher occurrence of renal problems, therefore close examination of the infant may be warranted shortly after birth. Among SUA infants, there is a slightly elevated risk for post-natal urinary infections.

It may be associated with Edwards syndrome.

It can be diagnosed with CT scan, angiography, transesophageal echocardiography, or cardiac MRI. Unfortunately, less invasive and expensive testing, such as transthoracic echocardiography and CT scanning are generally less sensitive.

Surgical treatment is best, when it can be performed. Pressure within the portal vein is measured as the shunt is closed, and it must be kept below 20 cm HO or else portal hypertension will ensue. Methods of shunt attenuation should aim to slowly occlude the vessel over several weeks to months in order to avoid complications associated with portal hypertension. These methods include ameroid ring constrictors, cellophane banding, intravascular or percutaneous silicone hydraulic occluders. The most common methods of attenuation used by veterinarians are ameroid ring constrictors and cellophane banding. Both methods have reportedly good outcomes in both cats and dogs, although the true composition of readily sourced cellophane has been found to be made from plastics (inert) and not cellulose (stimulates a fibrous reaction). Recently, a commercial supplier of regenerated cellulose based cellophane for veterinarians has been established for use of cellophane banding for portosystemic shunts in dogs and cats. Complete closure of extrahepatic shunts results in a very low recurrence rate, while incomplete closure results in a recurrence rate of about 50 percent. However, not all dogs with extrahepatic shunts tolerate complete closure (16 to 68 percent). Intrahepatic shunts are much more difficult to surgically correct than extrahepatic shunts due to their hidden nature, large vessel size, and greater tendency toward portal hypertension when completely closed. When surgery is not an option, PSS is treated as are other forms of liver failure. Dietary protein restriction is helpful to lessen signs of hepatic encephalopathy, and antibiotics such as neomycin or metronidazole and other medicines such as lactulose can reduce ammonia production and absorption in the intestines. The prognosis is guarded for any form of PSS.

This is based on MRI scan, magnetic resonance angiography and CT scan. A cerebral digital subtraction angiography (DSA) enhances visualization of the fistula.

- CT scans classically show an enlarged superior ophthalmic vein, cavernous sinus enlargement ipsilateral (same side) as the abnormality and possibly diffuse enlargement of all the extraocular muscles resulting from venous engorgement.

- Selective arteriography is used to evaluate arteriovenous fistulas.

- High resolution digital subtraction angiography may help in classifying CCF into dural and direct type and thus formulate a strategy to treat it either by a balloon or coil or both with or without preservation of parent ipsilateral carotid artery.

Nutcracker syndrome can be diagnosed with:

- Left renal venography—considered to be the gold standard test.

- Computed tomography (CT).

- Abdominal ultrasonography—not definitive but has been found to be useful.

A "Partial anomalous pulmonary venous connection" (or "Partial anomalous pulmonary venous drainage" or "Partial anomalous pulmonary venous return") is a congenital defect where the left atrium is the point of return for the blood from some (but not all) of the pulmonary veins.

It is less severe than total anomalous pulmonary venous connection which is a life-threatening anomaly requiring emergent surgical correction, usually diagnosed in the first few days of life. Partial anomalous venous connection may be diagnosed at any time from birth to old age. The severity of symptoms, and thus the likelihood of diagnosis, varies significantly depending on the amount of blood flow through the anomalous connections. In less severe cases, with smaller amounts of blood flow, diagnosis may be delayed until adulthood, when it can be confused with other causes of pulmonary hypertension. There is also evidence that a significant number of mild cases are never diagnosed, or diagnosed incidentally. It is associated with other vascular anomalies, and some genetic syndromes such as Turner syndrome.

In PLSVC, the left brachiocephalic vein does not develop fully and the left upper limb and head & neck drain into the right atrium via the coronary sinus.

The variation, in isolation, is considered benign, but is very frequently associated with cardiac abnormalities (e.g. ventricular septal defect, atrioventricular septal defect) that have a significant mortality and morbidity. It is more frequent in patients with congenital heart defects.

Diagnosis is very difficult, and usually one of exclusion. SMA syndrome is thus considered only after patients have undergone an extensive evaluation of their gastrointestinal tract including upper endoscopy, and evaluation for various malabsorptive, ulcerative and inflammatory instestinal conditions with a higher diagnostic frequency. Diagnosis may follow x-ray examination revealing duodenal dilation followed by abrupt constriction proximal to the overlying SMA, as well as a delay in transit of four to six hours through the gastroduodenal region. Standard diagnostic exams include abdominal and pelvic computed tomography (CT) scan with oral and IV contrast, upper gastrointestinal series (UGI), and, for equivocal cases, hypotonic duodenography. In addition, vascular imaging studies such as ultrasound and contrast angiography may be used to indicate increased bloodflow velocity through the SMA or a narrowed SMA angle.

Despite multiple case reports, there has been controversy surrounding the diagnosis and even the existence of SMA syndrome since symptoms do not always correlate well with radiologic findings, and may not always improve following surgical correction. However, the reason for the persistence of gastrointestinal symptoms even after surgical correction in some cases has been traced to the remaining prominence of reversed peristalsis in contrast to direct peristalsis.

Since females between the ages of 10 and 30 are most frequently afflicted, it is not uncommon for physicians to initially and incorrectly assume that emaciation is a choice of the patient instead of a consequence of SMA syndrome. Patients in the earlier stages of SMA syndrome often remain unaware that they are ill until substantial damage to their health is done, since they may attempt to adapt to the condition by gradually decreasing their food intake or naturally gravitating toward a lighter and more digestible diet.

In anatomy, a persistent left superior vena cava (PLSVC) is the most common variation of the thoracic venous system, is prevalent in 0.3% of the population, and an embryologic remnant that results from a failure to involute.

Fleischer's syndrome is an extremely rare congenital anomaly characterized by displacement of the nipples, occasional polymastia, and hypoplasia of both kidneys.

The following table includes the main types of valvular stenosis and regurgitation. Major types of valvular heart disease not included in the table include mitral valve prolapse, rheumatic heart disease and endocarditis.

a combination of various vascular malformations. They are 'complex' because they involve a combination of two different types of vessels.

- CVM: capillary venous malformation

- CLM: capillary lymphatic malformation

- LVM: lymphatic venous malformation

- CLVM: capillary lymphatic venous malformation. CLVM is associated with Klippel-Trenaunay syndrome

- AVM-LM: Arteriovenous malformation- lymphatic malformation

- CM-AVM: capillary malformation- arteriovenous malformation

The main techniques of diagnosing SVCS are with chest X-rays (CXR), CT scans, transbronchial needle aspiration at bronchoscopy and mediastinoscopy. CXRs provide the ability to show mediastinal widening and may show the presenting primary cause of SVCS. CT scans should be contrast enhanced and be taken on the neck, chest, lower abdomen and pelvis. They may also show the underlying cause and the extent to which the disease has progressed.

Congenital stenosis of vena cava is a congenital anomaly in which the superior vena cava or inferior vena cava has an aberrant interruption or coarctation.

In some cases, it can be asymptomatic, and in other cases it can lead to fluid accumulation and cardiopulmonary collapse.

Delay in the diagnosis of SMA syndrome can result in fatal catabolysis (advanced malnutrition), dehydration, electrolyte abnormalities, hypokalemia, acute gastric rupture or intestinal perforation (from prolonged mesenteric ischemia), gastric distention, spontaneous upper gastrointestinal bleeding, hypovolemic shock, and aspiration pneumonia.

A 1-in-3 mortality rate for Superior Mesenteric Artery syndrome has been quoted by a small number of sources. However, after extensive research, original data establishing this mortality rate has not been found, indicating that the number is likely to be unreliable. While research establishing an official mortality rate may not exist, two recent studies of SMA syndrome patients, one published in 2006 looking at 22 cases and one in 2012 looking at 80 cases, show mortality rates of 0% and 6.3%, respectively. According to the doctors in one of these studies, the expected outcome for SMA syndrome treatment is generally considered to be excellent.

Sinus pericranii (SP) is a rare disorder characterized by a congenital (or occasionally, acquired) epicranial venous malformation of the scalp. Sinus pericranii is an abnormal communication between the intracranial and extracranial venous drainage pathways. Treatment of this condition has mainly been recommended for aesthetic reasons and prevention of hemorrhage.

In human anatomy, an azygos lobe is a congenital variation of the upper lobe of the right lung.It is seen in 1% of the population. Embryologically, it arises from an anomalous lateral course of the azygos vein in a pleural septum within the apical segment of the right upper lobe or in other words an azygos lobe is formed when the right posterior cardinal vein, one of the precursors of the azygos vein, fails to migrate over the apex of the lung and penetrates it instead, carrying along two pleural layers that invaginates into the upper portion of the right upper lobe . As it has no bronchi, veins and arteries of its own or corresponding alteration in the segmental architecture of the lung, so it is not a true (misnomer), or even accessory, pulmonary lobe, but rather an anatomically separated part of the upper lobe. It is usually an incidental finding on chest x-ray or computed tomography and is as such not associated with any morbidity but can cause technical problems in thoracoscopic procedures .