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

The most common cause of chronic venous insufficiency is reflux of the venous valves of superficial veins. This may in turn be caused by several conditions:

- Deep vein thrombosis (DVT), that is, blood clots in the deep veins. Chronic venous insufficiency caused by DVT may be described as postthrombotic syndrome.

- Superficial vein thrombosis.

- Phlebitis

- May–Thurner syndrome. This is a rare condition in which blood clots occur in the iliofemoral vein due to compression of the blood vessels in the leg. The specific problem is compression of the left common iliac vein by the overlying right common iliac artery. Many May-Thurner compressions are overlooked when there is no blood clot. More and more of them get nowadays diagnosed and treated (by stenting) due to advanced imaging techniques.

Deep and superficial vein thrombosis may in turn be caused by thrombophilia, which is an increased propensity of forming blood clots.

Arteriovenous fistula (an abnormal connection or passageway between an artery and a vein) may cause chronic venous insufficiency even with working vein valves.

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.

Signs and symptoms of PTS in the leg may include:

- pain (aching or cramping)

- heaviness

- itching or tingling

- swelling (edema)

- varicose veins

- brownish or reddish skin discoloration

- ulcer

These signs and symptoms may vary among patients and over time. With PTS, these symptoms typically are worse after walking or standing for long periods of time and improve with resting or elevating the leg.

PTS lowers a person's quality of life after DVT, specifically with regards to physical and psychological symptoms and limitations in daily activities.

Post-thrombotic syndrome (PTS), also called postphlebitic syndrome and venous stress disorder is a medical condition that may occur as a long-term complication of deep vein thrombosis (DVT).

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.

Nine in ten people with sinus thrombosis have a headache; this tends to worsen over the period of several days, but may also develop suddenly (thunderclap headache). The headache may be the only symptom of cerebral venous sinus thrombosis. Many patients have symptoms of stroke: inability to move one or more limbs, weakness on one side of the face or difficulty speaking. This does not necessarily affect one side of the body as in the more common "arterial" stroke.

40% of people have seizures, although it is more common in women who develop sinus thrombosis peripartum (in the period before and after giving birth). These are mostly seizures affecting only one part of the body and unilateral (occurring on one side), but occasionally the seizures are generalised and rarely they lead to status epilepticus (persistent or recurrent seizure activity for a long period of time).

In the elderly, many of the aforementioned symptoms may not occur. Common symptoms in the elderly with this condition are otherwise unexplained changes in mental status and a depressed level of consciousness.

The pressure around the brain may rise, causing papilledema (swelling of the optic disc) which may be experienced as visual obscurations. In severely raised intracranial pressure, the level of consciousness is decreased, the blood pressure rises, the heart rate falls and the patient assumes an abnormal posture.

The symptoms of pulmonary hypertension include the following:

Less common signs/symptoms include non-productive cough and exercise-induced nausea and vomiting. Coughing up of blood may occur in some patients, particularly those with specific subtypes of pulmonary hypertension such as heritable pulmonary arterial hypertension, Eisenmenger syndrome and chronic thromboembolic pulmonary hypertension. Pulmonary venous hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary arterial hypertension (PAH) typically does not.

Other typical signs of pulmonary hypertension include an accentuated pulmonary component of the second heart sound, a right ventricular third heart sound, and parasternal heave indicating a hypertrophied right atrium. Signs of systemic congestion resulting from right-sided heart failure include jugular venous distension, ascites, and hepatojugular reflux. Evidence of tricuspid insufficiency and pulmonic regurgitation is also sought and, if present, is consistent with the presence of pulmonary hypertension.

A venous ulcer tends to occur on the medial side of the leg, typically around the medial malleolus in the 'gaiter area' whereas arterial ulcer tends to occur on lateral side of the leg and over bony prominences. A venous ulcer is typically shallow with irregular sloping edges whereas an arterial ulcer can be deep and has a 'punched out' appearance. Venous ulcers are typically 'wet' with a moderate to heavy exudate whereas. Arterial ulcers are typically 'dry' and scabbed. The skin surrounding a venous ulcer may be edematous (swollen) and there may be evidence of varicose veins; the skin surrounding an arterial ulcer may be pale, cold, shiny and hairless. Both venous and arterial ulcers may be painful, however arterial ulcers tend to be more painful, especially with elevation of the leg, for example when in bed.

Pain may be the first noticed symptom. People with lipodermatosclerosis have tapering of their legs above the ankles, forming a constricting band resembling an inverted champagne bottle. In addition, there may be brownish-red pigmentation and induration.

Telangiectasias, also known as spider veins, are small dilated blood vessels near the surface of the skin or mucous membranes, measuring between 0.5 and 1 millimeter in diameter.

These dilated blood vessels can develop anywhere on the body but are commonly seen on the face around the nose, cheeks, and chin. Dilated blood vessels can also develop on the legs, although when they occur on the legs, they often have underlying venous reflux or "hidden varicose veins" (see "Venous reflux" below). When found on the legs, they are found specifically on the upper thigh, below the knee joint, and around the ankles.

Many patients who suffer with spider veins seek the assistance of physicians who specialize in vein care or peripheral vascular disease. These physicians are called vascular surgeons or phlebologists. More recently, interventional radiologists have started treating venous problems.

Some telangiectasias are due to developmental abnormalities that can closely mimic the behaviour of benign vascular neoplasms. They may be composed of abnormal aggregations of arterioles, capillaries, or venules. Because telangiectasias are vascular lesions, they blanch when tested with diascopy.

Telangiectasia is a component of the CREST variant of scleroderma, also known today as limited scleroderma (CREST is an acronym that stands for calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia).

Leg ulcerations may result from various pathologic processes. Common causes of leg ulcerations include inadequate blood flow and oxygen delivery to tissues as seen in peripheral arterial disease and venous stasis ulcerations. Additional causes include neutrophilic dermatoses such as pyoderma gangrenosum or Sweet syndrome; vasculitic processes such as cryoglobulinemia; calciphylaxis (often seen in people with end-stage kidney disease but may also occur with medications such as warfarin); cancers such as squamous cell carcinoma (Marjolin's ulcer) or myelodysplastic syndrome; neuropathy (e.g., diabetic peripheral neuropathy); or atypical infections such as nocardiosis, sporotrichosis, or mycobacterial infections.

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.

Cerebral venous sinus thrombosis (CVST) is the presence of acute thrombosis (a blood clot) in the dural venous sinuses, which drain blood from the brain. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body, and seizures. The diagnosis is usually by computed tomography (CT/CAT scan) or magnetic resonance imaging (MRI) employing radiocontrast to demonstrate obstruction of the venous sinuses by thrombus.

Treatment is with anticoagulants (medication that suppresses blood clotting), and rarely thrombolysis (enzymatic destruction of the blood clot). Given that there is usually an underlying cause for the disease, tests may be performed to look for these. The disease may be complicated by raised intracranial pressure, which may warrant surgical intervention such as the placement of a shunt.

The clinical presentation of CST can be varied. Both acute, fulminant disease and indolent, subacute presentations have been reported in the literature.

The most common signs of CST are related to anatomical structures affected within the cavernous sinus, notably cranial nerves III-VI, as well as symptoms resulting from impaired venous drainage from the orbit and eye.

Classic presentations are abrupt onset of unilateral periorbital edema, headache, photophobia, and bulging of the eye (proptosis).

Other common signs and symptoms include:

Ptosis, chemosis, cranial nerve palsies (III, IV, V, VI). Sixth nerve palsy is the most common. Sensory deficits of the ophthalmic and maxillary branch of the fifth nerve are common. Periorbital sensory loss and impaired corneal reflex may be noted. Papilledema, retinal hemorrhages, and decreased visual acuity and blindness may occur from venous congestion within the retina. Fever, tachycardia and sepsis may be present. Headache with nuchal rigidity may occur. Pupil may be dilated and sluggishly reactive. Infection can spread to contralateral cavernous sinus within 24–48 hours of initial presentation.

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.

Arterial insufficiency ulcers (also known as Ischemic ulcers or Ischemic wounds) are mostly located on the lateral surface of the ankle or the distal digits. They are commonly caused by peripheral artery disease (PAD).

The causes of telangiectasia can be divided into congenital and acquired factors.

According to WHO classification there are 5 groups of PH, where Group I (pulmonary arterial hypertension) is further subdivided into Group I' and Group I" classes. The most recent WHO classification system (with adaptations from the more recent ESC/ERS guidelines shown in italics) can be summarized as follows:

WHO Group I – Pulmonary arterial hypertension (PAH)

- Idiopathic

- Heritable (BMPR2, ALK1, SMAD9, caveolin 1, KCNK3 mutations)

- Drug- and toxin-induced (e.g., methamphetamine use)

- Associated conditions:Connective tissue disease, HIV infection, Portal hypertension, Congenital heart diseases, Schistosomiasis

WHO Group I' – Pulmonary veno-occlusive disease (PVOD), pulmonary capillary hemangiomatosis (PCH)

- Idiopathic

- Heritable (EIF2AK4 mutations)

- Drugs, toxins and radiation-induced

- Associated conditions:connective tissue disease, HIV infection

WHO Group I" – Persistent pulmonary hypertension of the newborn

WHO Group II – Pulmonary hypertension secondary to left heart disease

- Left ventricular Systolic dysfunction

- Left ventricular Diastolic dysfunction

- Valvular heart disease

- Congenital/acquired left heart inflow/outflow tract obstruction and congenital cardiomyopathy

- Congenital/acquired pulmonary venous stenosis

WHO Group III – Pulmonary hypertension due to lung disease, chronic hypoxia

- Chronic obstructive pulmonary disease (COPD)

- Interstitial lung disease

- Mixed restrictive and obstructive pattern pulmonary diseases

- Sleep-disordered breathing

- Alveolar hypoventilation disorders

- Chronic exposure to high altitude

- Developmental abnormalities

WHO Group IV – chronic arterial obstruction

- Chronic thromboembolic pulmonary hypertension (CTEPH)

- Other pulmonary artery obstructions

- Angiosarcoma or other tumor within the blood vessels

- Arteritis

- Congenital pulmonary artery stenosis

- Parasitic infection (hydatidosis)

WHO Group V – Pulmonary hypertension with unclear or multifactorial mechanisms

- Hematologic diseases: chronic hemolytic anemia (including sickle cell disease)

- Systemic diseases: sarcoidosis, pulmonary Langerhans cell histiocytosis: lymphangioleiomyomatosis, neurofibromatosis, vasculitis

- Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid diseases

- Others: pulmonary tumoral thrombotic microangiopathy, fibrosing mediastinitis, chronic kidney failure, segmental pulmonary hypertension (pulmonary hypertension restricted to one or more lobes of the lungs)

The ulcer has punched-out appearance. It is intensely painful. It has gray or yellow fibrotic base and undermining skin margins. Pulses are not palpable. Associated skin changes may be observed, such as thin shiny skin and absence of hair. They are most common on distal ends of limbs. A special type of ischemic ulcer developing in duodenum after severe burns is called Curling's ulcer.

Lipodermatosclerosis (also known as "chronic panniculitis with lipomembranous changes", "hypodermitis sclerodermiformis", "sclerosing panniculitis", and "stasis panniculitis") is a skin and connective tissue disease. It is a form of lower extremity panniculitis, an inflammation of the layer of fat under the epidermis.

Cavernous sinus thrombosis (CST) is the formation of a blood clot within the cavernous sinus, a cavity at the base of the brain which drains deoxygenated blood from the brain back to the heart. The cause is usually from a spreading infection in the nose, sinuses, ears, or teeth. "Staphylococcus aureus" and "Streptococcus" are often the associated bacteria. Cavernous sinus thrombosis symptoms include: decrease or loss of vision, chemosis, exophthalmos (bulging eyes), headaches, and paralysis of the cranial nerves which course through the cavernous sinus. This infection is life-threatening and requires immediate treatment, which usually includes antibiotics and sometimes surgical drainage.

Acroangiodermatitis of Mali (also known as "Mali acroangiodermatitis" and "Pseudo-Kaposi's sarcoma") is a rare cutaneous condition often characterized by purplish-blue to brown papules and plaques on the medial and lateral malleolus of both legs.

Acroangiodermatitis is a rare skin condition characterised by hyperplasia of pre-existing vasculature due to venous hypertension from severe chronic venous stasis. It is associated with amputees, haemodialysis (HD) patients with arteriovenous (AV) shunts, and patients with paralysed legs, hepatitis C, chronic venous insufficiency or AV malformations (AVM). Patients present with itchy, painful, confluent, violaceous or brown-black macules, papules or plaques usually at the distal lower limbs. There may be ulceration and bleeding. The histologic features are capillary proliferation and perivascular inflammation involving eosinophils in the dermis with minimal epidermal changes. Management includes compression therapy, wound care and surgical correction of AVM. Dapsone combined with leg elevation and compression, and erythromycin for HD patients with AV fistulas have also been reported. The lesions may persist for years with complications like ulceration, bleeding and infection.