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

Anorectal varices are the dilation of collateral submucosal vessels due to backflow in the veins of the rectum. Typically this occurs due to portal hypertension which shunts venous blood from the portal system through the portosystemic anastomosis present at this site into the systemic venous system. This can also occur in the oesophagus, causing oesophageal varices, and at the level of the umbilicus, causing caput medusae. Between 44% and 78% of patients with portal hypertension get anorectal varices.

Most varicose veins are reasonably benign, but severe varicosities can lead to major complications, due to the poor circulation through the affected limb.

- Pain, tenderness, heaviness, inability to walk or stand for long hours, thus hindering work

- Skin conditions / dermatitis which could predispose skin loss

- Skin ulcers especially near the ankle, usually referred to as venous ulcers.

- Development of carcinoma or sarcoma in longstanding venous ulcers. Over 100 reported cases of malignant transformation have been reported at a rate reported as 0.4% to 1%.

- Severe bleeding from minor trauma, of particular concern in the elderly.

- Blood clotting within affected veins, termed superficial thrombophlebitis. These are frequently isolated to the superficial veins, but can extend into deep veins, becoming a more serious problem.

- Acute fat necrosis can occur, especially at the ankle of overweight people with varicose veins. Females are more frequently affected than males.

Varicose veins are veins that have become enlarged and twisted. The term commonly refers to the veins on the leg, although varicose veins can occur elsewhere. Veins have pairs of leaflet valves to prevent blood from flowing backwards (retrograde flow or venous reflux). Leg muscles pump the veins to return blood to the heart (the skeletal-muscle pump), against the effects of gravity. When veins become varicose, the leaflets of the valves no longer meet properly, and the valves do not work (valvular incompetence). This allows blood to flow backwards and they enlarge even more. Varicose veins are most common in the superficial veins of the legs, which are subject to high pressure when standing. Besides being a cosmetic problem, varicose veins can be painful, especially when standing. Severe long-standing varicose veins can lead to leg swelling, venous eczema, skin thickening (lipodermatosclerosis) and ulceration. Although life-threatening complications are uncommon, varicose veins may be confused with deep vein thrombosis, which may be life-threatening.

Non-surgical treatments include sclerotherapy, elastic stockings, leg elevation and exercise. The traditional surgical treatment has been vein stripping to remove the affected veins. Newer, less invasive treatments which seal the main leaking vein are available. Alternative techniques, such as ultrasound-guided foam sclerotherapy, radiofrequency ablation and endovenous laser treatment, are available as well. Because most of the blood in the legs is returned by the deep veins, the superficial veins, which return only about 10% of the total blood of the legs, can usually be removed or ablated without serious harm.

Secondary varicose veins are those developing as collateral pathways, typically after stenosis or occlusion of the deep veins, a common sequel of extensive deep venous thrombosis (DVT). Treatment options are usually support stockings, occasionally sclerotherapy and rarely, limited surgery.

Varicose veins are distinguished from reticular veins (blue veins) and telangiectasias (spider veins), which also involve valvular insufficiency, by the size and location of the veins. Many patients who suffer with varicose veins seek out the assistance of physicians who specialize in vein care or peripheral vascular disease. These physicians include vascular surgeons, phlebologists or interventional radiologists.

Esophageal varices (sometimes spelled oesophageal varices) are extremely dilated sub-mucosal veins in the lower third of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding. Esophageal varices are typically diagnosed through an esophagogastroduodenoscopy.

The terms rectal varices and haemorrhoids are often used interchangeably, but this is not correct. Haemorrhoids occur due to prolapse of the rectal venous plexus and are no more common in patients with portal hypertension than those without. Rectal varices, however, are only found in patients with portal hypertension and are common in conditions such as cirrhosis.

If not thrombosed, external hemorrhoids may cause few problems. However, when thrombosed, hemorrhoids may be very painful. Nevertheless, this pain typically resolves in two to three days. The swelling may, however, take a few weeks to disappear. A skin tag may remain after healing. If hemorrhoids are large and cause issues with hygiene, they may produce irritation of the surrounding skin, and thus itchiness around the anus.

Internal hemorrhoids usually present with painless, bright red rectal bleeding during or following a bowel movement. The blood typically covers the stool (a condition known as hematochezia), is on the toilet paper, or drips into the toilet bowl. The stool itself is usually normally coloured. Other symptoms may include mucous discharge, a perianal mass if they prolapse through the anus, itchiness, and fecal incontinence. Internal hemorrhoids are usually only painful if they become thrombosed or necrotic.

Arteriovenous malformations (AVMs, larger vascular malformations) occur in larger organs, predominantly the lungs (50%), liver (30–70%) and the brain (cerebral AVMs, 10%), with a very small proportion (<1%) having AVMs in the spinal cord.

Vascular malformations in the lungs may cause a number of problems. The lungs normally "filter out" bacteria and blood clots from the bloodstream; AVMs bypass the capillary network of the lungs and allow these to migrate to the brain, where bacteria may cause a brain abscess and blood clots may lead to stroke. HHT is the most common cause of lung AVMs: out of all people found to have lung AVMs, 70–80% are due to HHT. Bleeding from lung AVMs is relatively unusual, but may cause hemoptysis (coughing up blood) or hemothorax (blood accumulating in the chest cavity). Large vascular malformations in the lung allow oxygen-depleted blood from the right ventricle to bypass the alveoli, meaning that this blood does not have an opportunity to absorb fresh oxygen. This may lead to breathlessness. Large AVMs may lead to platypnea, difficulty in breathing that is more marked when sitting up compared to lying down; this probably reflects changes in blood flow associated with positioning. Very large AVMs cause a marked inability to absorb oxygen, which may be noted by cyanosis (bluish discoloration of the lips and skin), clubbing of the fingernails (often encountered in chronically low oxygen levels), and a humming noise over the affected part of the lung detectable by stethoscope.

The symptoms produced by AVMs in the liver depend on the type of abnormal connection that they form between blood vessels. If the connection is between arteries and veins, a large amount of blood bypasses the body's organs, for which the heart compensates by increasing the cardiac output. Eventually congestive cardiac failure develops ("high-output cardiac failure"), with breathlessness and leg swelling among other problems. If the AVM creates a connection between the portal vein and the blood vessels of the liver, the result may be portal hypertension (increased portal vein pressure), in which collateral blood vessels form in the esophagus (esophageal varices), which may bleed violently; furthermore, the increased pressure may give rise to fluid accumulation in the abdominal cavity (ascites). If the flow in the AVM is in the other direction, portal venous blood flows directly into the veins rather than running through the liver; this may lead to hepatic encephalopathy (confusion due to portal waste products irritating the brain). Rarely, the bile ducts are deprived of blood, leading to severe cholangitis (inflammation of the bile ducts). Liver AVMs are detectable in over 70% of people with HHT, but only 10% experience problems as a result.

In the brain, AVMs occasionally exert pressure, leading to headaches. They may also increase the risk of seizures, as would any abnormal tissue in the brain. Finally, hemorrhage from an AVM may lead to intracerebral hemorrhage (bleeding into the brain), which causes any of the symptoms of stroke such as weakness in part of the body or difficulty speaking. If the bleeding occurs into the subarachnoid space (subarachnoid hemorrhage), there is usually a severe, sudden headache and decreased level of consciousness and often weakness in part of the body.

Telangiectasia (small vascular malformations) may occur in the skin and mucosal linings of the nose and gastrointestinal tract. The most common problem is nosebleeds (epistaxis), which happen frequently from childhood and affect about 90–95% of people with HHT. Lesions on the skin and in the mouth bleed less often but may be considered cosmetically displeasing; they affect about 80%. The skin lesions characteristically occur on the lips, the nose and the fingers, and on the skin of the face in sun-exposed areas. They appear suddenly, with the number increasing over time.

About 20% are affected by symptomatic digestive tract lesions, although a higher percentage have lesions that do not cause symptoms. These lesions may bleed intermittently, which is rarely significant enough to be noticed (in the form of bloody vomiting or black stool), but can eventually lead to depletion of iron in the body, resulting in iron-deficiency anemia.

Most patients with portal hypertensive gastropathy have either a stable or improving course in the appearance of the gastropathy on endoscopy. However, according to retrospective data, roughly one in seven patients with portal hypertensive gastropathy will develop bleeding (either acute or chronic) attributable to the gastropathy. Patients with chronic bleeding will usually come to the attention of the medical system because of anemia.

The diagnosis of portal hypertensive gastropathy is usually made on endoscopy. The usual appearance of portal hypertensive gastropathy on endoscopy is a mosaic-like or reticular pattern in the mucosa. Red spots may or may not be present. The pattern is usually seen throughout the stomach. A similar pattern can be seen with a related condition called gastric antral vascular ectasia (GAVE), or watermelon stomach. However, in GAVE, the ectatic blood vessels are more commonly found in the antrum or lower part of the stomach.

Gastric varices can present in two major ways. First, patients with cirrhosis may be enrolled in screening gastroscopy programs to detect esophageal varices. These evaluations may detect gastric varices that are asymptomatic. When gastric varices are symptomatic, however, they usually present acutely and dramatically with upper gastrointestinal bleeding. The symptoms can include vomiting blood, melena (passing black, tarry stools); or passing maroon stools or frank blood in the stools. Many people with bleeding gastric varices present in shock due to the profound loss of blood.

Secondly, patients with acute pancreatitis may present with gastric varices as a complication of a blood clot in the splenic vein. The splenic vein sits over the pancreas anatomically and inflammation or cancers of the pancreas may result in a blot clot forming in the splenic vein. As the short gastric veins of the fundus of the stomach drain into the splenic vein, thrombosis of the splenic vein will result in increased pressure and engorgement of the short veins, leading to varices in the fundus of the stomach.

Laboratory testing usually shows low red blood cell count and often a low platelet count. If cirrhosis is present, there may be coagulopathy manifested by a prolonged INR; both of these may worsen the bleeding from gastric varices.

In very rare cases, gastric varices are caused by splenic vein occlusion as a result of the mass effect of slow-growing pancreatic neuroendocrine tumors.

Portal hypertensive gastropathy refers to changes in the mucosa of the stomach in patients with portal hypertension; by far the most common cause of this is cirrhosis of the liver. These changes in the mucosa include friability of the mucosa and the presence of ectatic blood vessels at the surface. Patients with portal hypertensive gastropathy may experience bleeding from the stomach, which may uncommonly manifest itself in vomiting blood or melena; however, portal hypertension may cause several other more common sources of upper gastrointestinal bleeding, such as esophageal varices and gastric varices. On endoscopic evaluation of the stomach, this condition shows a characteristic mosaic or "snake-skin" appearance to the mucosa of the stomach.

Gastric varices are dilated submucosal veins in the stomach, which can be a life-threatening cause of bleeding in the upper gastrointestinal tract. They are most commonly found in patients with portal hypertension, or elevated pressure in the portal vein system, which may be a complication of cirrhosis. Gastric varices may also be found in patients with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow. The latter may be a complication of acute pancreatitis, pancreatic cancer, or other abdominal tumours, as well as hepatitis C. Gastric varices and associated bleeding are a potential complication of schistosomiasis resulting from portal hypertension.

Patients with bleeding gastric varices can present with bloody vomiting (hematemesis), dark, tarry stools (melena), or rectal bleeding. The bleeding may be brisk, and patients may soon develop shock. Treatment of gastric varices can include injection of the varices with cyanoacrylate glue, or a radiological procedure to decrease the pressure in the portal vein, termed transjugular intrahepatic portosystemic shunt or TIPS. Treatment with intravenous octreotide is also useful to shunt blood flow away from the stomach's circulation. More aggressive treatment including splenectomy (or surgical removal of the spleen) or liver transplantation may be required in some cases.

Caviar tongue (also termed sublingual varicosities or sublingual varices), is a condition characterized by purplish venous ectasias commonly found on the ventral (undersurface) of the tongue after the age of fifty. It is normal for there to be veins visible underneath the tongue, partly because the mucous membrane is so thin and translucent in this region, but where these vessels become dilated and tortuous, they may appear round and black like caviar.

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.

Intestinal varices are dilated submucosal veins in the intestine.

One treatment includes a transjugular intrahepatic portosystemic shunt.

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.

Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.

A spider angioma (also known as a nevus araneus, spider nevus, vascular spider, and spider telangiectasia) is a type of telangiectasis (swollen blood vessels) found slightly beneath the skin surface, often containing a central red spot and reddish extensions which radiate outwards like a spider's web. They are common and may be benign, presenting in around 10–15% of healthy adults and young children. However, having more than three spider angiomas is likely to be abnormal and may be a sign of liver disease. It also suggests the probability of esophageal varices.

Spider angiomas are found only in the distribution of the superior vena cava, and are thus commonly found on the face, neck, upper part of the trunk, and arms. They may also be present on the backs of the hands and fingers in young children.

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).

Fistulas can develop in various parts of the body. The following list is sorted by the International Statistical Classification of Diseases and Related Health Problems.

In medicine, ovarian vein syndrome is a rare (possibly not uncommon, certainly under-diagnosed) condition in which a dilated ovarian vein compresses the ureter (the tube that brings the urine from the kidney to the bladder). This causes chronic or colicky abdominal pain, back pain and/or pelvic pain. The pain can worsen on lying down or between ovulation and menstruation. There can also be an increased tendency towards urinary tract infection or pyelonephritis (kidney infection). The right ovarian vein is most commonly involved, although the disease can be left-sided or affect both sides. It is currently classified as a form of pelvic congestion syndrome.

A fistula is an abnormal connection between two hollow spaces (technically, two epithelialized surfaces), such as blood vessels, intestines, or other hollow organs. Fistulas are usually caused by injury or surgery, but they can also result from an infection or inflammation. Fistulas are generally a disease condition, but they may be surgically created for therapeutic reasons.

In botany, the term is most common in its adjectival forms, where it is used in binomial names to refer to species that are distinguished by hollow or tubular structures. Monarda fistulosa, for example, has tubular flowers; Eutrochium fistulosum has a tubular stem; and Allium fistulosum has hollow or tubular leaves.