Treatment is focused on reducing stroke episodes and damage from a distending artery. Four treatment modalities have been reported in the treatment of vertebral artery dissection. The two main treatments involve medication: anticoagulation (using heparin and warfarin) and antiplatelet drugs (usually aspirin). More rarely, thrombolysis (medication that dissolves blood clots) may be administered, and occasionally obstruction may be treated with angioplasty and stenting. No randomized controlled trials have been performed to compare the different treatment modalities. Surgery is only used in exceptional cases.

From analysis of the existing small treatment trials of cervical artery dissection (carotid and vertebral) it appears that aspirin and anticoagulation (heparin followed by warfarin) are equally effective in reducing the risk of further stroke or death. Anticoagulation is regarded as more powerful than antiplatelet therapy, but anticoagulants may increase the size of the hematoma and worsen obstruction of the affected artery. Anticoagulation may be relatively unsafe if a large stroke has already occurred, as hemorrhagic transformation is relatively common, and if the dissection extends into V4 (carrying a risk of subarachnoid hemorrhage). Anticoagulation may be appropriate if there is rapid blood flow (through a severely narrowed vessel) on transcranial doppler despite the use of aspirin, if there is a completely occluded vessel, if there are recurrent stroke-like episodes, or if free-floating blood clot is visible on scans. Warfarin is typically continued for 3–6 months, as during this time the flow through the artery usually improves, and most strokes happen within the first 6 months after the development of the dissection. Some regard 3 months as sufficient.

Professional guidelines in the UK recommend that patients with VA dissection should be enrolled in a clinical trial comparing aspirin and anticoagulation if possible. American guidelines state that the benefit of anticoagulation is not currently established.

Evidence for the treatment of thoracic outlet syndrome as of 2014 is poor.

Surgical approaches have also been used successfully in TOS. Microsurgery can be used approaching the area from above the collar bone (supraclavicular) followed by neurolysis of the brachial plexus, removal of the scalene muscle (scalenectomy), and the release of the underlying (subclavicular) blood vessels. This approach avoids the use of resection, and has been found to be an effective treatment. In cases where the first rib (or a fibrous band extending from the first rib) is compressing a vein, artery, or the nerve bundle, part of the first rib and any compressive fibrous tissue, can be removed in a first rib resection surgical procedure; scalene muscles may also need to be removed (scalenectomy). This allows increased blood flow and the reduction of nerve compression. In some cases there may be a rudimentary rib or a cervical rib that can be causing the compression, which can be removed using the same technique.

Physical therapy is often used before and after the operation to improve recovery time and outcomes. Potential complications include pneumothorax, infection, loss of sensation, motor problems, subclavian vessel damage, and, as in all surgeries, a very small risk of permanent serious injury or death.

The goal of treatment is to prevent the development or continuation of neurologic deficits. Treatments include observation, anticoagulation, stent implantation and carotid artery ligation.

Surgical treatment involves resection of the stenosed segment and re-anastomsis. Two complications specific to this surgery are Left recurrent nerve palsy and chylothorax, as the recurrent laryngeal nerve and thoracic duct are in the vicinity. Chylothorax is a troublesome complication and is usually managed conservatively by adjusting the diet to eliminate long chain fatty acids and supplementing medium chain triglycerides. When conservative management fails surgical intervention is required. Fluorescein dye can aid in the localisation of chyle leak.

The treatment of arterial tortuosity syndrome entails possible surgery for aortic aneurysms, as well as, follow ups which should consist of EGC. The prognosis of this condition has it at about 12% mortality

In adults and children found to have coarctation, treatment is conservative if asymptomatic, but may require surgical resection of the narrow segment if there is arterial hypertension. The first operations to treat coarctation were carried out by Clarence Crafoord in Sweden in 1944. In some cases angioplasty can be performed to dilate the narrowed artery, with or without the placement of a stent graft.

For fetuses at high risk for developing coarctation, a novel experimental treatment approach is being investigated, wherein the mother inhales 45% oxygen three times a day (3 x 3–4 hours) beyond 34 weeks of gestation. The oxygen is transferred via the placenta to the fetus and results in dilatation of the fetal lung vessels. As a consequence, the flow of blood through the fetal circulatory system increases, including that through the underdeveloped arch. In suitable fetuses, marked increases in aortic arch dimensions have been observed over treatment periods of about two to three weeks.

The long term outcome is very good. Some patients may, however, develop narrowing (stenosis) or dilatation at the previous coarctation site. All patients with unrepaired or repaired aortic coarctation require follow up in specialized Congenital Heart Disease centers.

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.

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).

Treatment is usually supportive as persistent bleeding is uncommon. However cauterization or injection of epinephrine to stop the bleeding may be undertaken during the index endoscopy procedure. Very rarely embolization of the arteries supplying the region may be required to stop the bleeding. If all other methods fail, high gastrostomy can be used to ligate the bleeding vessel. It is to be noted that the tube will not be able to stop bleeding as here the bleeding is arterial and the pressure in the balloon is not sufficient to overcome the arterial pressure.

Early treatment is essential to keep the affected limb viable. The treatment options include injection of an anticoagulant, thrombolysis, embolectomy, surgical revascularisation, or amputation. Anticoagulant therapy is initiated to prevent further enlargement of the thrombus. Continuous IV unfractionated heparin has been the traditional agent of choice.

If the condition of the ischemic limb is stabilized with anticoagulation, recently formed emboli may be treated with catheter-directed thrombolysis using intraarterial infusion of a thrombolytic agent (e.g., recombinant tissue plasminogen activator (tPA), streptokinase, or urokinase). A percutaneous catheter inserted into the femoral artery and threaded to the site of the clot is used to infuse the drug. Unlike anticoagulants, thrombolytic agents work directly to resolve the clot over a period of 24 to 48 hours.

Direct arteriotomy may be necessary to remove the clot. Surgical revascularization may be used in the setting of trauma (e.g., laceration of the artery). Amputation is reserved for cases where limb salvage is not possible. If the patient continues to have a risk of further embolization from some persistent source, such as chronic atrial fibrillation, treatment includes long-term oral anticoagulation to prevent further acute arterial ischemic episodes.

Decrease in body temperature reduces the aerobic metabolic rate of the affected cells, reducing the immediate effects of hypoxia. Reduction of body temperature also reduces the inflammation response and reperfusion injury. For frostbite injuries, limiting thawing and warming of tissues until warmer temperatures can be sustained may reduce reperfusion injury.

Treatment for Larsen syndrome varies according to the symptoms of the individual. Orthopedic surgery can be performed to correct the serious joint defects associated with Larsen syndrome. Reconstructive surgery can be used to treat the facial abnormalities. Cervical kyphosis can be very dangerous to an individual because it can cause the vertebrae to disturb the spinal cord. Posterior cervical arthrodesis has been performed on patients with cervical kyphosis, and the results have been successful Propranolol has been used to treat some of the cardiac defects associated with Marfan's syndrome, so the drug also has been suggested to treat cardiac defects associated with Larsen syndrome.

The surgery takes place under general anaesthesia and lasts less than 1 hour. The surgeon prepares the locus to the size of the implant after performing a 8-cm axillary incision and inserts the implant beneath the skin. The closure is made in 2 planes.

The implant will replace the pectoralis major muscle, thus enabling the thorax to be symmetrical and, in women, the breast as well. If necessary, especially in the case of women, a second operation will complement the result by the implantation of a breast implant and / or lipofilling.

Lipomodelling is progressively used in the correction of breast and chest wall deformities. In Poland syndrome, this technique appears to be a major advance that will probably revolutionize the treatment of severe cases. This is mainly due to its ability to achieve previously unachievable quality of reconstruction with minimal scaring.

The complete or partial absence of the pectoralis muscle is the malformation that defines Poland Syndrome. It can be treated by inserting a custom implant designed by CAD (computer aided design). A 3D reconstruction of the patient's chest is performed from a medical scanner to design a virtual implant perfectly adapted to the anatomy of each one. The implant is made of medical silicone unbreakable rubber. This treatment is purely cosmetic and does not make up for the patient's imbalanced upper body strength.

The Poland syndrome malformations being morphological, correction by custom implant is a first-line treatment. This technique allows a wide variety of patients to be treated with good outcomes. Poland Syndrome can be associated with bones, subcutaneous and mammary atrophy: if the first, as for pectus excavatum, is successfully corrected by a custom implant, the others can require surgical intervention such as lipofilling or silicone breast implant, in a second operation.

While Larsen syndrome can be lethal if untreated, the prognosis is relatively good if individuals are treated with orthopedic surgery, physical therapy, and other procedures used to treat the symptoms linked with Larsen syndrome.

Treatment for Klippel–Feil syndrome is symptomatic and may include surgery to relieve cervical or craniocervical instability and constriction of the spinal cord, and to correct scoliosis.

Failing non-surgical therapies, spinal surgery may provide relief. Adjacent segment disease and scoliosis are two examples of common symptoms associated with Klippel–Feil syndrome, and they may be treated surgically. The three categories treated for types of spinal cord deficiencies are massive fusion of the cervical spine (Type I), the fusion of 1 or 2 vertebrae (Type II), and the presence of thoracic and lumbar spine anomalies in association with type I or type II Klippel–Feil syndrome (Type III).

Adjacent segment disease can be addressed by performing cervical disc arthroplasty using a device such as the Bryan cervical disc prosthesis.

The option of the surgery is to maintain range of motion and attenuate the rate of adjacent segment disease advancement without fusion.

Another type of arthroplasty that is becoming an alternate choice to spinal fusion is Total Disc Replacement. Total disc replacement objective is to reduce pain or eradicate it.

Spinal fusion is commonly used to correct spinal deformities such as scoliosis. Arthrodesis is the last resort in pain relieving procedures, usually when arthroplasties fail.

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.

Doctors often recommend physical therapy in order to strengthen the subscapularis muscle, and prescribe anti-inflammatory medications. For extreme cases, cortisone injections would be utilized.

Surgery is usually only used if the non-surgical treatments have failed. Bone abnormalities may need surgical attention. The most common surgery for snapping scapula requires the surgeon to “take out a small piece of the upper corner of the scapula nearest to the spine.”

With the exception of a few case reports describing survival without surgery, the mortality of untreated Boerhaave syndrome is nearly 100%. Its treatment includes immediate antibiotic therapy to prevent mediastinitis and sepsis, surgical repair of the perforation, and if there is significant fluid loss it should be replaced with IV fluid therapy since oral rehydration is not possible. Even with early surgical intervention (within 24 hours) the risk of death is 25%.

Non specific thoracic spine pain is usually treated by one or a combination of the following:

- Exercise/Active and passive physical therapy

- Deep massage or massage therapy

- Ice and/or heat therapy

- Analgesics such as non-steroidal anti-inflammatory drugs

- Joint manipulation, as commonly performed by physical therapists, chiropractors or osteopathic physicians (D.O.).

- If there is a specific tender spot, then trigger point massage or injections can be helpful.

A painful vertebral compression fracture may be treated with pain medication and rest, or with vertebroplasty or kyphoplasty surgery. If the cause is thought to be osteoporosis, oral or intravenous bisphosphonates may be administered to reduce further fracture risk.

Currently the only definitive treatment is liver transplantation. Alternative treatments such as supplemental oxygen or somatostatin to inhibit vasodilation remain anecdotal.

Usually the hemangioma requires medical therapy. The child may need other therapies, depending on what other organs or structures are involved.

Treatment is symptomatic, often addressing indicators associated with peripheral pulmonary artery stenosis. Laryngotracheal calcification resulting in dyspnea and forceful breathing can be treated with bronchodilators including the short and long-acting β2-agonists, and various anticholinergics. Prognosis is good, yet life expectancy depends on the severity and extent of diffuse pulmonary and arterial calcification.