Treatments include anticoagulants, shunts, bypass surgery, and transplants.

Anticoagulation, which prevents further coagulation, but does not act directly on existing clots, is the standard treatment for DVT. Balancing risk vs. benefit is important in determining the duration of anticoagulation, and three months is generally the standard length of treatment. In those with an annual risk of VTE in excess of 9%, as after an unprovoked episode, extended anticoagulation is a possibility. Those who finish VKA treatment after idiopathic VTE with an elevated D-dimer level show an increased risk of recurrent VTE (about 9% vs about 4% for normal results), and this result might be used in clinical decision-making. Thrombophilia test results rarely play a role in the length of treatment.

For acute cases in the leg, the ACCP recommended a parenteral anticoagulant (such as LMWH, fondaparinux, or unfractionated heparin) for at least five days and a VKA, the oral anticoagulant, the same day. LMWH and fondaparinux are suggested over unfractionated heparin, but both are retained in those with compromised kidney function, unlike unfractionated heparin. The VKA is generally taken for a minimum of three months to maintain an international normalized ratio of 2.0–3.0, with 2.5 as the target. The benefit of taking a VKA declines as the duration of treatment extends, and the risk of bleeding increases with age.

The ACCP recommended treatment for three months in those with proximal DVT provoked by surgery. A three-month course is also recommended for those with proximal DVT provoked by a transient risk factor, and three months is suggested over lengthened treatment when bleeding risk is low to moderate. Unprovoked DVT patients should have at least three months of anticoagulation and be considered for extended treatment. Those whose first VTE is an unprovoked proximal DVT are suggested for anticoagulation longer than three months unless there is a high risk of bleeding. In that case, three months is sufficient. Those with a second unprovoked VTE are recommended for extended treatment when bleeding risk is low, suggested for extended treatment when bleeding risk is moderate, and suggested for three months of anticoagulation in high-risk scenarios.

The ACCP recommended initial home treatment instead of hospital treatment for those with acute leg DVT. This applies as long as individuals feel ready for it, and those with severe leg symptoms or comorbidities would not qualify. An appropriate home environment is expected: one that can provide a quick return to the hospital if necessary, support from family or friends, and phone access.

In addition to anticoagulation, the ACCP suggested graduated compression stockings—which apply higher pressure (30–40 mm Hg) at the ankles and a lower pressure around the knees—for those with symptomatic DVT. Use should begin as soon as possible after anticoagulation. Evidence however does not support that these stockings reduce the risk of post-thrombotic syndrome nor do they indicate a reduction in recurrent VTE. Use is suggested for two years, though inconvenience and discomfort can reduce compliance. Walking is also suggested for those without severe pain or edema.

Unless a person has medical problems preventing movement, after a person starts anti-coagulation therapy bed rest should not be used to treat acute deep vein thrombosis. There are clinical benefits associated with walking and no evidence that walking is harmful, but people with DVT are harmed by bed rest except when it is medically necessary.

Instead of anticoagulation, a follow-up imaging test (typically ultrasound) about one-week post-diagnosis is an option for those with an acute isolated distal DVT without a high risk for extension; if the clot does not grow, the ACCP does not recommend anticoagulation. This technique can benefit those at a high risk for bleeding. Patients may choose anticoagulation over serial imaging, however, to avoid the inconvenience of another scan if concerns about the risk of bleeding are insignificant. When applied to symptomatic patients with a negative initial ultrasound result, serial testing is inefficient and not cost effective.

Warfarin and vitamin K antagonists are anticoagulants that can be taken orally to reduce thromboembolic occurrence. Where a more effective response is required, heparin can be given (by injection) concomitantly. As a side effect of any anticoagulant, the risk of bleeding is increased, so the international normalized ratio of blood is monitored. Self-monitoring and self-management are safe options for competent patients, though their practice varies. In Germany, about 20% of patients were self-managed while only 1% of U.S. patients did home self-testing (according to one 2012 study). Other medications such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used instead of warfarin.

Recommendations for those without cancer include anticoagulation (stopping further blood clots from forming) with dabigatran, rivaroxaban, apixaban, or edoxaban rather than warfarin or low molecular weight heparin (LMWH). For those with cancer LMWH is recommended. For initial treatment of VTE, fixed doses with LMWH may be more effective than adjusted doses of unfractionated heparin (UFH) in reducing blood clots. No differences in mortality, prevention of major bleeding, or preventing VTEs from recurring were observed between LMWH and UFH. No differences have been detected in the route of administration of UFH (subcutaneous or intravenous). LMWH is usually administered by a subcutaneous injection, and a persons blood clotting factors do not have to be monitored as closely as with UFH. People with cancer have a higher risk of experiencing reoccurring VTE episodes ("recurrent VTE"), despite taking preventative anticoagulation medication. These people should be given therapeutic doses of LMWH medication, either by switching from another anticoagulant or by taking a higher dose of LMWH.

For those with a small pulmonary embolism and few risk factors, no anticoagulation is needed. Anticoagulation is; however, recommended in those who do have risk factors. Thrombolysis is recommended in those with PEs that are causing low blood pressure.

Evidence-based clinical guidelines were published in 2016 for the treatment of VTE.

Thrombolysis is the pharmacological destruction of blood clots by administering thrombolytic drugs including recombitant tissue plasminogen activator, which enhances the normal destruction of blood clots by the body's enzymes. This carries an increased risk of bleeding so is generally only used for specific situations (such as severe stroke or a massive pulmonary embolism).

In terms of treatment for this condition the individual may be advised to do the following: "raise" the affected area to decrease swelling, and relieve pressure off of the affected area so it will encounter less pain. In certain circumstances drainage of the clot might be an option. In general, treatment may include the following:

Treatment with compression stockings should be offered to patients with lower extremity superficial phlebitis, if not contraindicated (e.g., peripheral artery disease). Patients may find them helpful for reducing swelling and pain once the acute inflammation subsides.

Nonsteroidal anti-inflammatory drugs (NSAID) are effective in relieving the pain associated with venous inflammation and were found in a randomized trial to significantly decrease extension and/or recurrence of superficial vein thrombosis.

Anticoagulation for patients with lower extremity superficial thrombophlebitis at increased risk for thromboembolism (affected venous segment of ≥5 cm, in proximity to deep venous system, positive medical risk factors).

Treatment with fondaparinux reduces the risk of subsequent venous thromboembolism.

Surgery reserved for extension of the clot to within 1 cm of the saphenofemoral junction in patients deemed unreliable for anticoagulation, failure of anticoagulation and patients with intense pain. Surgical therapy with ligation of saphenofemoral junction or stripping of thrombosed superficial veins appears to be associated higher rates of venous thromboembolism compared with treatment with anitcoagulants.

Various studies have investigated the use of anticoagulation to suppress blood clot formation in cerebral venous sinus thrombosis. Before these trials had been conducted, there had been a concern that small areas of hemorrhage in the brain would bleed further as a result of treatment; the studies showed that this concern was unfounded. Clinical practice guidelines now recommend heparin or low molecular weight heparin in the initial treatment, followed by warfarin, provided there are no other bleeding risks that would make these treatments unsuitable. Some experts discourage the use of anticoagulation if there is extensive hemorrhage; in that case, they recommend repeating the imaging after 7–10 days. If the hemorrhage has decreased in size, anticoagulants are started, while no anticoagulants are given if there is no reduction.

The duration of warfarin treatment depends on the circumstances and underlying causes of the condition. If the thrombosis developed under temporary circumstances (e.g. pregnancy), three months are regarded as sufficient. If the condition was unprovoked but there are no clear causes or a "mild" form of thrombophilia, 6 to 12 months is advised. If there is a severe underlying thrombosis disorder, warfarin treatment may need to continue indefinitely.

Thrombolysis (removal of the blood clot with "clot buster" medication) has been described, either systemically by injection into a vein or directly into the clot during angiography. The 2006 European Federation of Neurological Societies guideline recommends that thrombolysis is only used in patients who deteriorate despite adequate treatment, and other causes of deterioration have been eliminated. It is unclear which drug and which mode of administration is the most effective. Bleeding into the brain and in other sites of the body is a major concern in the use of thrombolysis. American guidelines make no recommendation with regards to thrombolysis, stating that more research is needed.

Raised intracranial pressure, if severe or threatening vision, may require therapeutic lumbar puncture (removal of excessive cerebrospinal fluid), medication (acetazolamide), or neurosurgical treatment (optic nerve sheath fenestration or shunting). In certain situations, anticonvulsants may be used to try to prevent seizures. These situations include focal neurological problems (e.g. inability to move a limb) and focal changes of the brain tissue on CT or MRI scan. Evidence to support or refute the use of antiepileptic drugs as a preventive measure, however, is lacking.

Treatment for Thrombotic Storm may include lifelong anticoagulation therapy and/or thrombolytic therapy, plasmapherisis, and corticosteroids. Studies have shown that when anticoagulant therapy is withheld recurrence of thrombosis usually follows. INR is closely monitored in the course of treatment.

A treatment plan may involve lactulose, enemas, and use of antibiotics such as rifaximin, neomycin, vancomycin, and the quinolones. Restriction of dietary protein was recommended but this is now refuted by a clinical trial which shows no benefit. Instead, the maintenance of adequate nutrition is now advocated.

Both pharmacological (non-specific β-blockers, nitrate isosorbide mononitrate, vasopressin such as terlipressin) and endoscopic (banding ligation) treatment have similar results. TIPS (transjugular intrahepatic portosystemic shunting) is effective at reducing the rate of rebleeding.

The management of active variceal bleeding includes administering vasoactive drugs (somatostatin, octreotide), endoscopic banding ligation, balloon tamponade and TIPS.

There is no specific treatment for thrombophilia, unless it is caused by an underlying medical illness (such as nephrotic syndrome), where the treatment of the underlying disease is needed. In those with unprovoked and/or recurrent thrombosis, or those with a high-risk form of thrombophilia, the most important decision is whether to use anticoagulation medications, such as warfarin, on a long-term basis to reduce the risk of further episodes. This risk needs to weighed against the risk that the treatment will cause significant bleeding, as the reported risk of major bleeding is over 3% per year, and 11% of those with major bleeding may die as a result.

Apart from the abovementioned forms of thrombophilia, the risk of recurrence after an episode of thrombosis is determined by factors such as the extent and severity of the original thrombosis, whether it was provoked (such as by immobilization or pregnancy), the number of previous thrombotic events, male sex, the presence of an inferior vena cava filter, the presence of cancer, symptoms of post-thrombotic syndrome, and obesity. These factors tend to be more important in the decision than the presence or absence of a detectable thrombophilia.

Those with antiphospholipid syndrome may be offered long-term anticoagulation after a first unprovoked episode of thrombosis. The risk is determined by the subtype of antibody detected, by the antibody titer (amount of antibodies), whether multiple antibodies are detected, and whether it is detected repeatedly or only on a single occasion.

Women with a thrombophilia who are contemplating pregnancy or are pregnant usually require alternatives to warfarin during pregnancy, especially in the first 13 weeks, when it may produce abnormalities in the unborn child. Low molecular weight heparin (LMWH, such as enoxaparin) is generally used as an alternative. Warfarin and LMWH may safely be used in breastfeeding.

When women experience recurrent pregnancy loss secondary to thrombophilia, some studies have suggested that low molecular weight heparin reduces the risk of miscarriage. When the results of all studies are analysed together, no statistically signifiant benefit could be demonstrated.

Surgery to remove the clot is possible, but rarely performed. In the past, surgical removal of the renal vein clot was the primary treatment but it is very invasive and many complications can occur. In the past decades, treatment has shifted its focus from surgical intervention to medical treatments that include intravenous and oral anticoagulants. The use of anticoagulants may improve renal function in RVT cases by removing the clot in the vein and preventing further clots from occurring. Patients already suffering from nephrotic syndrome may not need to take anticoagulants. In this case, patients should keep an eye out and maintain reduced level of proteinuria by reducing salt and excess protein, and intaking diuretics and statins. Depending on the severity of RVT, patients may be on anticoagulants from a year up to a lifetime. As long as the albumen levels in the bloodstream are below 2.5g/L, it is recommended that RVT patients continue taking anticoagulants. Main anticoagulants that can be used to treat RVT include warfarin and low molecular weight heparin. Heparin has become very popular, because of its low risk of complications, its availability and because it can easily be administered. Warfarin is known to interact with many other drugs, so careful monitoring is required. If a nephrotic syndrome patient experiences any of the RVT symptoms (flank or back pain, blood in the urine or decreased renal function), he or she should immediately see a doctor to avoid further complications.

The main side effect of anticoagulants is the risk of excessive bleeding. Other side effects include: blood in the urine or feces, severe bruising, prolonged nosebleeds (lasting longer than 10 minutes), bleeding gum, blood in your vomit or coughing up blood, unusual headaches, sudden severe back pain, difficulty breathing or chest pain, in women, heavy or increased bleeding during the period, or any other bleeding from the vagina. Warfarin can cause rashes, diarrhea, nausea (feeling sick) or vomiting, and hair loss. Heparin can cause hair loss (alopecia) thrombocytopenia – a sudden drop in the number of platelets in the blood.

It has been reported in a case study of 27 patients with nephrotic syndrome caused RVT, there was a 40% mortality rate, mostly due to hemorrhagic complications and sepsis. In 75% of the remaining surviving patients, the RVT was resolved and renal function returned to normal. It has been concluded that age is not a factor on the survival of RVT patients, although older patient (55 and older) are more likely to develop renal failure. Heparin is crucial in returning normal renal function; in patients that did not take heparin, long term renal damage was observed in 100%. In patients that did take heparin, renal damage was observed in about 33%. By quickly treating, and receiving the correct medications, patients should increase their chances of survival and reduce the risk of the renal vein clot from migrating to another part of the body.

Prevention consists of walking, drinking fluids and if currently hospitalized, changing of IV lines. Walking is especially suggested after a long period seated, particularly when one travels.

Treatment can be either conservative or active. Active treatments can be divided into surgical and non-surgical treatments. Newer methods including endovenous laser treatment, radiofrequency ablation and foam sclerotherapy appear to work as well as surgery for varices of the greater saphenous vein.

In ideal circumstances, patients with known varices should receive treatment to reduce their risk of bleeding. The non-selective β-blockers (e.g., propranolol, timolol or nadolol) and nitrates (e.g., isosorbide mononitrate (IMN) have been evaluated for secondary prophylaxis. Non-selective β-blockers (but not cardioselective β-blockers like atenolol) are preferred because they decrease both cardiac output by β blockade and splanchnic blood flow by blocking vasodilating β receptors at splanchnic vasculature. The effectiveness of this treatment has been shown by a number of different studies.

However, non-selective β-blockers do not prevent the "formation" of esophageal varices.

When medical contraindications to beta-blockers exist, such as significant reactive airway disease, then treatment with prophylactic endoscopic variceal ligation is often performed.

A minority of patients can be treated medically with sodium restriction, diuretics to control ascites, anticoagulants such as heparin and warfarin, and general symptomatic management. The majority of patients require further intervention. Milder forms of Budd–Chiari may be treated with surgical shunts to divert blood flow around the obstruction or the liver itself. Shunts must be placed early after diagnosis for best results. The TIPS is similar to a surgical shunt: it accomplishes the same goal but has a lower procedure-related mortality—a factor that has led to a growth in its popularity. If all the hepatic veins are blocked, the portal vein can be approached via the intrahepatic part of inferior vena cava, a procedure called DIPS (direct intrahepatic portocaval shunt). Patients with stenosis or vena caval obstruction may benefit from angioplasty. Limited studies on thrombolysis with direct infusion of urokinase and tissue plasminogen activator into the obstructed vein have shown moderate success in treating Budd–Chiari syndrome; however, it is not routinely attempted.

Liver transplantation is an effective treatment for Budd–Chiari. It is generally reserved for patients with fulminant liver failure, failure of shunts or progression of cirrhosis that reduces the life expectancy to 1 year. Long-term survival after transplantation ranges from 69–87%. The most common complications of transplant include rejection, arterial or venous thromboses and bleeding due to anticoagulation. Up to 10% of patients may have a recurrence of Budd–Chiari syndrome after the transplant.

The National Institute for Health and Clinical Excellence (NICE) produced clinical guidelines in July 2013 recommending that all people with symptomatic varicose veins (C2S) and worse should be referred to a vascular service for treatment. Conservative treatments such as support stockings should not be used unless treatment was not possible.

The symptoms of varicose veins can be controlled to an extent with the following:

- Elevating the legs often provides temporary symptomatic relief.

- Advice about regular exercise sounds sensible but is not supported by any evidence.

- The wearing of graduated compression stockings with variable pressure gradients (Class II or III) has been shown to correct the swelling, nutritional exchange, and improve the microcirculation in legs affected by varicose veins. They also often provide relief from the discomfort associated with this disease. Caution should be exercised in their use in patients with concurrent peripheral arterial disease.

- The wearing of intermittent pneumatic compression devices have been shown to reduce swelling and increase circulation

- Diosmin/hesperidin and other flavonoids.

- Anti-inflammatory medication such as ibuprofen or aspirin can be used as part of treatment for superficial thrombophlebitis along with graduated compression hosiery – but there is a risk of intestinal bleeding. In extensive superficial thrombophlebitis, consideration should be given to anti-coagulation, thrombectomy, or sclerotherapy of the involved vein.

- Topical gel application helps in managing symptoms related to varicose veins such as inflammation, pain, swelling, itching, and dryness.

In emergency situations, care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics such as quinolones or ceftriaxone. Blood volume resuscitation should be done promptly and with caution. The goal should be hemodynamic stability and hemoglobin of over 8 g/dl. Resuscitation of all lost blood leads to increase in portal pressure leading to more bleeding. Volume resuscitation can also worsen ascites and increase portal pressure. (AASLD guidelines)

Therapeutic endoscopy is considered the mainstay of urgent treatment. The two main therapeutic approaches are variceal ligation or banding and sclerotherapy.

In cases of refractory bleeding, balloon tamponade with a Sengstaken-Blakemore tube may be necessary, usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (usually portal hypertension). Esophageal devascularization operations such as the Sugiura procedure can also be used to stop complicated variceal bleeding. Methods of treating the portal hypertension include: transjugular intrahepatic portosystemic shunt, or a distal splenorenal shunt procedure or a liver transplantation.

Nutritional supplementation is not necessary if the patient is not eating for four days or less.

Terlipressin and octreotide for 1 to 5 days have also been used.

Treatment usually consists of NSAIDs, such as ibuprofen and local compression (e.g., by compression stockings or a compress). If the phlebitis is associated with local bacterial infection, antibiotics may be used.

For acute infusion superficial thrombophlebitis, not enough evidence exists as of 2015 to determine treatment.

Several treatment options have been developed for portal hypertensive gastropathy. The first is the use of beta-blockers, which reduce portal pressures. Non-selective beta blockers (such as propranolol and nadolol) have been used to decrease the pressure of the portal vein in patients with esophageal varices, and have been shown to regress portal hypertensive gastropathy that has been worsened by medical treatment of varices. Propranolol has also been evaluated in patients with chronic cirrhosis and portal hypertensive gastropathy. Other medications that primarily treat bleeding, including anti-fibrinolytic medications such as tranexamic acid have also been used in case reports of patients with portal hypertensive gastropathy. These medications work by stabilizing deposits of fibrin at sites that ordinarily would bleed.

Finally, octreotide, an analogue of somatostatin that leads to vasoconstriction of the portal circulation, can be used for active bleeding due to portal hypertensive gastropathy. Sucralfate, a coating medication has also been used, but evidence is from animal models.

Given the fact that HIT predisposes strongly to new episodes of thrombosis, it is not sufficient to simply discontinue the heparin administration. Generally, an alternative anticoagulant is needed to suppress the thrombotic tendency while the generation of antibodies stops and the platelet count recovers. To make matters more complicated, the other most commonly used anticoagulant, warfarin, should not be used in HIT until the platelet count is at least 150 x 10^9/L because there is a very high risk of warfarin necrosis in people with HIT who have low platelet counts. Warfarin necrosis is the development of skin gangrene in those receiving warfarin or a similar vitamin K inhibitor. If the patient was receiving warfarin at the time when HIT is diagnosed, the activity of warfarin is reversed with vitamin K. Transfusing platelets is discouraged, as there is a theoretical risk that this may worsen the risk of thrombosis; the platelet count is rarely low enough to be the principal cause of significant hemorrhage.

Various non-heparin agents are used to provide anticoagulation in those with strongly suspected or proven HIT: danaparoid, fondaparinux, bivalirudin and argatroban. These are alternatives to heparin therapy. Not all agents are available in all countries, and not all are approved for this specific use. For instance, argatroban is only recently licensed in the United Kingdom, and danaparoid is not available in the United States. Fondaparinux, a Factor Xa inhibitor, is commonly used off label for HIT treatment in the United States.

According to a systematic review, people with HIT treated with lepirudin showed a relative risk reduction of clinical outcome (death, amputation, etc.) to be 0.52 and 0.42 when compared to patient controls. In addition, people treated with argatroban for HIT showed a relative risk reduction of the above clinical outcomes to be 0.20 and 0.18. Lepirudin production stopped on May 31, 2012.

As there is no cure, treatment is focused on prevention of thrombotic complications by counseling. In addition, temporary treatment with an anticoagulant may be required during periods of particularly high risk of thrombosis, such as major surgery.