Vein of Galen malformations are devastating complications. Studies have shown that 77% of untreated cases result in mortality. Even after surgical treatment, the mortality rate remains as high as 39.4%. Most cases occur during infancy when the mortality rates are at their highest. Vein of Galen malformations are a relatively unknown affliction, attributed to the rareness of the malformations. Therefore, when a child is diagnosed with a faulty Great Cerebral Vein of Galen, most parents know little to nothing about what they are dealing with. To counteract this, support sites have been created which offer information, advice, and a community of support to the afflicted (, ).

The complications that are usually associated with vein of Galen malformations are usually intracranial hemorrhages. Over half the patients with VGAM have a malformation that cannot be corrected. Patients frequently die in the neonatal period or in early infancy.

10-15% of intracranial AV malformations are DAVFs. There is a higher preponderance in females (61-66%), and typically patients are in their fourth or fifth generation of life. DAVFs are rarer in children.

Manual carotid self compression is a controversial treatment for DAVF. Patients using this method are told to compress the carotid with the opposite hand for approximately 10 minutes daily, and gradually increasing the frequency and duration of compression. Currently, it is unclear whether this method is an effective therapy.

A cirsoid aneurysm is the dilation of a group of blood vessels due to congenital malformations with AV (arterio venous) shunting. Cirsoid means resembling a varix.

Sometimes, a minor traumatic episode, such as a fall or bump on the head, can lead to the formation of a cirsoid aneurysm. Often these are trivial traumatic episodes

Cirsoid aneurysm, in general, is a hemangioma of an artery. It most commonly occurs over the head, usually the superficial temporal artery and also its branches. It can also occur in places where medium vessels lie over bones without much intervening tissues between them and the skin.

The superficial temporal artery is the most commonly involved artery.

When an arteriovenous fistula is formed involving a major artery like the abdominal aorta, it can lead to a large decrease in peripheral resistance. This lowered peripheral resistance causes the heart to increase cardiac output to maintain proper blood flow to all tissues. The physical manifestations of this would be a relatively normal systolic blood pressure with a decreased diastolic blood pressure resulting in a wide pulse pressure.

Normal blood flow in the brachial artery is 85 to 110 milliliters per minute (mL/min). After the creation of a fistula, the blood flow increases to 400–500 mL/min immediately, and 700–1,000 mL/min within 1 month. A bracheocephalic fistula above the elbow has a greater flow rate than a radiocephalic fistula at the wrist. Both the artery and the vein dilate and elongate in response to the greater blood flow and shear stress, but the vein dilates more and becomes "arterialized". In one study, the cephalic vein increased from 2.3 mm to 6.3 mm diameter after 2 months. When the vein is large enough to allow cannulation, the fistula is defined as "mature".

An arteriovenous fistula can increase preload. AV shunts also decrease the afterload of the heart. This is because the blood bypasses the arterioles which results in a decrease in the total peripheral resistance (TPR). AV shunts increase both the rate and volume of blood returning to the heart.

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.

The intrahepatic shunts found in large dog breeds are passed on in a simple autosomal recessive way, while the extrahepatic shunts of the small breeds are inherited on a polygenic basis.

Just like berry aneurysm, an intracerebral arteriovenous fistula can rupture causing subarachnoid hemorrhage.

DVA can be diagnosed through the Cerebral venous sinus thrombosis with collateral drainage. DVA can also be found diagnosed with Sturge–Weber syndrome and can be found through leptomeningeal angiomatosis. Demyelinating disease has also been found to enlarge Medulla veins.

Treatment depends on the severity and symptoms. Treatments include:

- Endovascular stenting.

- Renal vein re-implantation.

- Gonadal vein embolization.

A developmental venous anomaly (DVA, formerly known as venous angioma) is a congenital variant of the cerebral venous drainage. On imaging it is seen as a number of small deep parenchymal veins converging toward a larger collecting vein.

May-Thurner syndrome (MTS) is thought to represent between two and five percent of lower-extremity venous disorders. May-Thurner syndrome is often unrecognized; however, current estimates are that this condition is three times more common in women than in men. The classic syndrome typically presents in the second to fourth decades of life. In the 21st century in a broader disease profile, the syndrome acts as a permissive lesion and becomes symptomatic when something else happens such as, following trauma, a change in functional status such as swelling following orthopaedic joint replacement.

It is important to consider May-Thurner syndrome in patients who have no other obvious reason for hypercoagulability and who present with left lower extremity thrombosis. To rule out other causes for hypercoagulation, it may be appropriate to check the antithrombin, protein C, protein S, factor V Leiden, and prothrombin G20210A.

Venography will demonstrate the classical syndrome when causing deep venous thrombosis.

May-Thurner syndrome in the broader disease profile known as nonthrombotic iliac vein lesions (NIVLs) exists in the symptomatic ambulatory patient and these lesions are usually not seen by venography. Morphologically, intravascular ultrasound (IVUS) has emerged as the best current tool in the broader sense. Functional testing such as duplex ultrasound, venous and interstitial pressure measurement and plethysmography may sometimes be beneficial. Compression of the left common iliac vein may be seen on pelvic CT.

Management of the underlying defect is proportional to the severity of the clinical presentation. Leg swelling and pain is best evaluated by vascular specialists (vascular surgeons, interventional cardiologists, interventional radiologists) who both diagnose and treat arterial and venous diseases to ensure that the cause of the extremity pain is evaluated. The diagnosis needs to be confirmed with some sort of imaging that may include magnetic resonance venography, venogram and usually confirmed with intravascular ultrasound because the flattened vein may not be noticed on conventional venography. In order to prevent prolonged swelling or pain from the consequences of the backed up blood from the compressed iliac vein, flow needs to be improved out of the leg. Uncomplicated cases may be managed with compression stockings.

Severe May-Thurner syndrome may require thrombolysis if there is a recent onset of thrombosis, followed by angioplasty and stenting of the iliac vein after confirming the diagnosis with a venogram or an intravascular ultrasound. A stent may be used to support the area from further compression following angioplasty. As the name implies, there classically is not a thrombotic component in these cases, but thrombosis may occur at any time.

If the patient has extensive thrombosis, it may be appropriate to consider pharmacologic and/or mechanical (also known as pharmacomechanical) thrombectomy. This is currently being studied to determine whether this will decrease the incidence of post-thrombotic syndrome.

The nutcracker syndrome (NCS) results most commonly from the compression of the left renal vein between the abdominal aorta (AA) and superior mesenteric artery (SMA), although other variants exist. The name derives from the fact that, in the sagittal plane and/or transverse plane, the SMA and AA (with some imagination) appear to be a nutcracker crushing a nut (the renal vein).

There is a wide spectrum of clinical presentations and diagnostic criteria are not well defined, which frequently results in delayed or incorrect diagnosis.

This condition is not to be confused with superior mesenteric artery syndrome, which is the compression of the third portion of the duodenum by the SMA and the AA.

Pulmonary vein stenosis is a rare cardiovascular disorder. It is recognized as being the stenosis of one or more of the four pulmonary veins that return blood from the lungs to the left atrium of the heart. In congenital cases, it is associated with poor prognosis and high mortality rate. In some people, pulmonary vein stenosis occurs after pulmonary vein ablation for the treatment of atrial fibrillation. Some recent research has indicated that it may be genetically linked in congenital cases.

Vascular occlusion is a blockage of a blood vessel, usually with a clot. It differs from thrombosis in that it can be used to describe any form of blockage, not just one formed by a clot. When it occurs in a major vein, it can, in some cases, cause deep vein thrombosis. The condition is also relatively common in the retina, and can cause partial or total loss of vision. An occlusion can often be diagnosed using Doppler sonography (a form of ultrasound).

Some medical procedures, such as embolisation, involve occluding a blood vessel to treat a particular condition. This can be to reduce pressure on aneurysms (weakened blood vessels) or to restrict a haemorrhage. It can also be used to reduce blood supply to tumours or growths in the body, and therefore restrict their development. Occlusion can be carried out using a ligature; by implanting small coils which stimulate the formation of clots; or, particularly in the case of cerebral aneurysms, by clipping.

Several studies have attempted to predict the survival of patients with Budd–Chiari syndrome. In general, nearly 2/3 of patients with Budd–Chiari are alive at 10 years. Important negative prognostic indicators include ascites, encephalopathy, elevated Child-Pugh scores, elevated prothrombin time, and altered serum levels of various substances (sodium, creatinine, albumin, and bilirubin). Survival is also highly dependent on the underlying cause of the Budd–Chiari syndrome. For example, a patient with an underlying myeloproliferative disorder may progress to acute leukemia, independently of Budd–Chiari syndrome.

It is known that diabetes causes changes to factors associated with coagulation and clotting, however not much is known of the risk of thromboembolism, or clots, in diabetic patients. There are some studies that show that diabetes increases the risk of thromboembolism; other studies show that diabetes does not increase the risk of thromboembolism. A study conducted in the Umea University Hospital, in Sweden, observed patients that were hospitalized due to an thromboembolism from 1997 to 1999. The researchers had access to patient information including age, sex, vein thromboembolism diagnosis, diagnostic methods, diabetes type and medical history. This study concluded that there is, in fact, an increased risk of thromboembolism development in diabetic patients, possibly due to factors associated with diabetes or diabetes itself. Diabetic patients are twice as likely to develop a thromboembolism than are non-diabetic patient. The exact mechanism of how diabetes increases the risk of clot formation remains unclear and could possibly be a future direction for study.

From previous studies, it is known that long distance air travel is associated with high risk of venous thrombosis. Long periods of inactivity in a limited amount of space may be a reason for the increased risk of blood clot formation. In addition, bent knees compresses the vein behind the knee (the popliteal vein) and the low humidity, low oxygen, high cabin pressure and consumption of alcohol concentrate the blood. A recent study, published in the British Journal of Haematology in 2014, determined which groups of people, are most at risk for developing a clot during or after a long flight. The study focused on 8755 frequent flying employees from international companies and organizations. It found that travelers who have recently undergone a surgical procedure or who have a malignant disease such as cancer or who are pregnant are most at risk. Preventative measures before flying may be taken in these at-risk groups as a solution.

Patients who have undergone kidney transplant have a high risk of developing RVT (about 0.4% to 6%). RVT is known to account for a large proportion of transplanted kidney failures due to technical problems (damage to the renal vein), clotting disorders, diabetes, consumption of ciclosporin or an unknown problem. Patients who have undergone a kidney transplant are commonly prescribed ciclosporin, an immunosuppressant drug which is known to reduce renal blood flow, increase platelet aggregation in the blood and cause damage to the endothelial tissue of the veins. In a clinical study conducted by the Nuffield Department of Surgery at the Oxford Transplant Centre, UK, transplant patients were given low doses of aspirin, which has a some anti-platelet activity. There is risk of bleeding in transplant patients when using anticoagulants like warfarin and herapin. Low dosage of aspirin was used as an alternative. The study concluded that a routine low-dose of aspirin in kidney transplant patients who are also taking ciclosporin significantly reduces the risk of RVT development.

Jugular vein ectasia is a venous anomaly that commonly presents itself as a unilateral neck swelling in children and adults. It is rare to have bilateral neck swelling due to internal jugular vein ectasia.

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.

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 .

A varix (pl. varices) is an abnormally dilated vessel with a tortuous course. Varices usually occur in the venous system, but may also occur in arterial or lymphatic vessels.

Examples of varices include:

- Varicose veins, large tortuous veins usually found on legs

- Sublingual varices

- Esophageal varices, commonly stemming from cirrhosis of the liver, also known as oesophageal varicose

- Gastric varices, commonly stemming from cirrhosis of the liver

- Intestinal varices

- Scrotal varices

- Vulvar varices

- Pelvic varices

- Vesical varices, varicose veins associated with the urinary bladder

- Rectal varices, which can be similar to external haemorrhoids

Annuloaortic ectasia is a dilation of the proximal ascending aorta and aortic annulus. It may cause aortic regurgitation, thoracic aortic dissection, aneurysm and rupture. It is often associated with connective tissue diseases like Marfan syndrome and Ehlers Danlos Syndrome. It can also be a complication due to tertiary syphilis. In tertiary syphilis the aortic root becomes so dilated that the aortic valve becomes incompetent and cor bovinum results.

The term was first coined by the American heart surgeon Denton Cooley in 1961.

The average age of diagnosis for GAVE is 73 years of age for females, and 68 for males. Women are about twice as often diagnosed with gastric antral vascular ectasia than men. 71% of all cases of GAVE are diagnosed in females. Patients in their thirties have been found to have GAVE. It becomes more common in women in their eighties, rising to 4% of all such gastrointestinal conditions.

5.7% of all sclerosis patients (and 25% of those who had a certain anti-RNA marker) have GAVE.