Vein of Galen aneurysmal malformations (VGAM) and Vein of Galen aneurysmal dilations (VGAD) are the most frequent arteriovenous malformations in infants and fetuses. VGAM consist of a tangled mass of dilated vessels supplied by an enlarged artery. The malformation increases greatly in size with age, although the mechanism of the increase is unknown. Dilation of the great cerebral vein of Galen is a secondary result of the force of arterial blood either directly from an artery via an arteriovenous fistula or by way of a tributary vein that receives the blood directly from an artery. There is usually a venous anomaly downstream from the draining vein that, together with the high blood flow into the great cerebral vein of Galen causes its dilation. The right sided cardiac chambers and pulmonary arteries also develop mild to severe dilation.

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.

The most common signs/symptoms of DAVFs are:

1. Pulsatile tinnitus

2. Occipital bruit

3. Headache

4. Visual impairment

5. Papilledema

Pulsatile tinnitus is the most common symptom in patients, and it is associated with transverse-sigmoid sinus DAVFs. Carotid-cavernous DAVFs, on the other hand, are more closely associated with pulsatile exophthalmos. DAVFs may also be asymptomatic (e.g. cavernous sinus DAVFs).

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.

Most commonly found adjacent to dural sinuses in the following locations:

1. Transverse (lateral) sinus, left-sided slightly more common than right

2. Intratentorial

3. From the posterior cavernous sinus, usually draining to the transverse or sigmoid sinuses

4. Vertebral artery (posterior meningeal branch)

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.

DVA can be characterized by the Caput medusae sign of veins, which drains into a larger vein. The drains will either drain into a Dural venous sinuses or into a deep ependymal vein. It appears to look like a Palm tree.

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.

NCS is associated with hematuria (which can lead to anemia) and abdominal pain (classically left flank or pelvic pain).

Since the left gonadal vein drains via the left renal vein it can also result in left testicular pain in men or left lower quadrant pain in women. Nausea and vomiting can result due to compression of the splanchnic veins. An unusual manifestation of NCS includes varicocele formation and varicose veins in the lower limbs. Another clinical study has shown that nutcracker syndrome is a frequent finding in varicocele-affected patients and possibly, nutcracker syndrome should be routinely excluded as a possible cause of varicocele and pelvic congestion.

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.

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

An arteriovenous fistula is an abnormal connection or passageway between an artery and a vein. It may be congenital, surgically created for hemodialysis treatments, or acquired due to pathologic process, such as trauma or erosion of an arterial aneurysm.

In medicine, May-Thurner syndrome (MTS), also known as the iliac vein compression syndrome, is a rare condition in which compression of the common venous outflow tract of the left lower extremity may cause discomfort, swelling, pain or blood clots, called deep venous thrombosis (DVT), in the iliofemoral vein.

The specific problem is compression of the left common iliac vein by the overlying right common iliac artery. This leads to pooling or stasis of blood, predisposing the individual to the formation of blood clots. Uncommon variations of MTS have been described, such as the right common iliac vein getting compressed by the right common iliac artery.

In the 21st century the May-Thurner syndrome definition has been expanded to a broader disease profile known as nonthrombotic iliac vein lesions (NIVL) which can involve both the right and left iliac veins as well as multiple other named venous segments. This syndrome frequently manifests as pain when the limb is dependent (hanging down the edge of a bed/chair) and/or significant swelling of the whole limb.

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.

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.

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.

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 .

The acute syndrome presents with rapidly progressive severe upper abdominal pain, yellow discoloration of the skin and whites of the eyes, liver enlargement, enlargement of the spleen, fluid accumulation within the peritoneal cavity, elevated liver enzymes, and eventually encephalopathy. The fulminant syndrome presents early with encephalopathy and ascites. Liver cell death and severe lactic acidosis may be present as well. Caudate lobe enlargement is often present. The majority of patients have a slower-onset form of Budd–Chiari syndrome. This can be painless. A system of venous collaterals may form around the occlusion which may be seen on imaging as a "spider's web". Patients may progress to cirrhosis and show the signs of liver failure.

On the other hand, incidental finding of a silent, asymptomatic form may not be a cause for concern.

Budd–Chiari syndrome is a very rare condition, affecting 1 in a million adults. The condition is caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of abdominal pain, ascites, and liver enlargement. The formation of a blood clot within the hepatic veins can lead to Budd–Chiari syndrome. The syndrome can be fulminant, acute, chronic, or asymptomatic.

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.

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

Signs and symptoms of CVI in the leg include the following:

- Varicose veins

- Itching (pruritus)

- Hyperpigmentation

- Phlebetic lymphedema

- Chronic swelling of the legs and ankles

- Venous ulceration

CVI in the leg may cause the following:

- Venous stasis

- Ulcers.

- Stasis dermatitis, also known as varicose eczema

- Contact dermatitis. Patients with venous insufficiency have a disrupted epidermal barrier, making them more susceptible than the general population to contact sensitization and subsequent dermatitis.

- Atrophie blanche. This is an end point of a variety of conditions, appears as atrophic plaques of ivory white skin with telangiectasias. It represents late sequelae of lipodermatosclerosis where the skin has lost its nutrient blood flow.

- Lipodermatosclerosis. This is an indurated plaque in the medial malleolus.

- Malignancy. Malignant degeneration is a rare but important complication of venous disease since tumors which develop in the setting of an ulcer tend to be more aggressive.

- Pain. Pain is a feature of venous disease often overlooked and commonly undertreated.

- Anxiety.

- Depression.

- Inflammation

- Discoloration

- Skin thickening

- Cellulitis

A Zahn infarct is a pseudo-infarction of the liver, consisting of an area of congestion with parenchymal atrophy but no necrosis, and usually due to obstruction of a branch of the portal vein. Zahn infarcts are unique in that there is collateral congestion of liver sinusoids that do not include areas of anoxia seen in most infarcts. Fibrotic tissue may develop in the area of the infarct and it could be caused by an occlusive phlebitis in portal vein radicles. Non ischemic infarct of liver with lines of Zahn.

Cruveilhier–Baumgarten disease or Pégot-Cruveilhier–Baumgarten disease is a rare medical condition in which the umbilical or paraumbilical veins are distended, with an abdominal wall bruit (the Cruveilhier-Baumgarten bruit) and palpable thrill, portal hypertension with splenomegaly, hypersplenism and oesophageal varices, with a normal or small liver.

It was first described by Pégot in 1833, and then by Jean Cruveilhier (1835) and Paul Clemens von Baumgarten (1907).

Armstrong "et al." (1942) and Steinburg and Galambos (1967) described two different types of the condition:

- Cruveilhier-Baumgarten syndrome: liver cirrhosis or portal hypertension is the cause of the distension of the paraumbilical veins (i.e. an "acquired" condition in which the veins reopen due to high portal pressure).

- Cruveilhier–Baumgarten disease: the distension of the paraumbilical veins is due to failure of umbilical vein closure, with little or no evidence of liver disease found on liver biopsy (i.e. a "congenital" patency of the umbilical vein leading to portal hypertension).