Adson's sign and the costoclavicular maneuver lack specificity and sensitivity and should comprise only a small part of the mandatory comprehensive history and physical examination undertaken with a patient suspected of having TOS. There is currently no single clinical sign that makes the diagnosis of TOS with any degree of certainty.

Additional maneuvers that may be abnormal in TOS include Wright's Test, which involves hyperabducting the arms over the head with some extension and evaluating for loss of radial pulses or signs of blanching of the skin in the hands indicating a decrease in blood flow with the maneuver. The "compression test" is also used, exerting pressure between the clavicle and medial humeral head causes radiation of pain and/or numbness into the affected arm.

Doppler arteriography, with probes at the fingertips and arms, tests the force and "smoothness" of the blood flow through the radial arteries, with and without having the patient perform various arm maneuvers (which causes compression of the subclavian artery at the thoracic outlet). The movements can elicit symptoms of pain and numbness and produce graphs with diminished arterial blood flow to the fingertips, providing strong evidence of impingement of the subclavian artery at the thoracic outlet. Doppler arteriography does not utilize probes at the fingertips and arms, and in this case is likely being confused with plethysmography, which is a different method that utilizes ultrasound without direct visualization of the affected vessels. It should also be noted that Doppler ultrasound (not really 'arteriography') would not be used at the radial artery in order to make the diagnosis of TOS. Finally, even if a Doppler study of the appropriate artery were to be positive, it would not diagnose neurogenic TOS, by far the most common subtype of TOS. There is plenty of evidence in the medical literature to show that arterial compression does not equate to brachial plexus compression, although they may occur together, in varying degrees. Additionally, arterial compression by itself does not make the diagnosis of arterial TOS (the rarest form of TOS). Lesser degrees of arterial compression have been shown in normal individuals in various arm positions and are thought to be of little significance without the other criteria for arterial TOS.

Various diagnostic modalities exist to demonstrate blood flow or absence thereof in the vertebral arteries. The gold standard is cerebral angiography (with or without digital subtraction angiography). This involves puncture of a large artery (usually the femoral artery) and advancing an intravascular catheter through the aorta towards the vertebral arteries. At that point, radiocontrast is injected and its downstream flow captured on fluoroscopy (continuous X-ray imaging). The vessel may appear stenotic (narrowed, 41–75%), occluded (blocked, 18–49%), or as an aneurysm (area of dilation, 5–13%). The narrowing may be described as "rat's tail" or "string sign". Cerebral angiography is an invasive procedure, and it requires large volumes of radiocontrast that can cause complications such as kidney damage. Angiography also does not directly demonstrate the blood in the vessel wall, as opposed to more modern modalities. The only remaining use of angiography is when endovascular treatment is contemplated (see below).

More modern methods involve computed tomography (CT angiography) and magnetic resonance imaging (MR angiography). They use smaller amounts of contrast and are not invasive. CT angiography and MR angiography are more or less equivalent when used to diagnose or exclude vertebral artery dissection. CTA has the advantage of showing certain abnormalities earlier, tends to be available outside office hours, and can be performed rapidly. When MR angiography is used, the best results are achieved in the "T" setting using a protocol known as "fat suppression". Doppler ultrasound is less useful as it provides little information about the part of the artery close to the skull base and in the vertebral foramina, and any abnormality detected on ultrasound would still require confirmation with CT or MRI.

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 terms of the diagnosis of arterial tortuosity syndrome can be done via genetic testing, as well as the following listed below:

- CT

- MRI

- Echocardiogram

- Physical exam(for specific characteristics)

Prognosis of spontaneous cervical arterial dissection involves neurological and arterial results. The overall functional prognosis of individuals with stroke due to cervical artery dissection does not appear to vary from that of young people with stroke due to other causes. The rate of survival with good outcome (a modified Rankin score of 0–2) is generally about 75%, or possibly slightly better (85.7%) if antiplatelet drugs are used. In studies of anticoagulants and aspirin, the combined mortality with either treatment is 1.8–2.1%.

After the initial episode, 2% may experience a further episode within the first month. After this, there is a 1% annual risk of recurrence. Those with high blood pressure and dissections in multiple arteries may have a higher risk of recurrence. Further episodes of cervical artery dissection are more common in those who are younger, have a family history of cervical artery dissection, or have a diagnosis of Ehlers-Danlos syndrome or fibromuscular dysplasia.

Unfortunately, coarctations can not be prevented because they are usually present at birth. The best thing for patients who are affected by coarctations is early detection. Some signs that can lead to a coarctation have been linked to pathologies such as Turner syndrome, bicuspid aortic valve, and other family heart conditions.

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.

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

Leaving the hospital after a coarctation procedure is only one step in a lifelong process. Just because the coarctation was fixed does not mean that the patient is cured. It is extremely important to visit the cardiologist on a regular basis. Depending on the severity of the patient's condition, which is evaluated on a case-by-case level, visiting a cardiologist can be a once a year surveillance check up. Keeping a regular schedule of appointments with a cardiologist after a coarctation procedure is complete helps increase the chances of survivability for the patients.

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

The use of heparin following surgery is common if there are no issues with bleeding. Generally, a risk-benefit analysis is required, as all anticoagulants lead to an increased risk of bleeding. In people admitted to hospital, thrombosis is a major cause for complications and occasionally death. In the UK, for instance, the Parliamentary Health Select Committee heard in 2005 that the annual rate of death due to thrombosis was 25,000, with at least 50% of these being hospital-acquired. Hence "thromboprophylaxis" (prevention of thrombosis) is increasingly emphasized. In patients admitted for surgery, graded compression stockings are widely used, and in severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend low molecular weight heparin (LMWH) administration, mechanical calf compression or (if all else is contraindicated and the patient has recently suffered deep vein thrombosis) the insertion of a vena cava filter. In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis, and in the United Kingdom the Chief Medical Officer has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines.

Pseudohypertension, also known as pseudohypertension in the elderly, noncompressibility artery syndrome, and Osler's sign of pseudohypertension is a falsely elevated blood pressure reading obtained through sphygmomanometry due to calcification of blood vessels which cannot be compressed. There is normal blood pressure when it is measured from within the artery. This condition however is associated with significant cardiovascular disease risk.

Because the stiffened arterial walls of arteriosclerosis do not compress with pressure normally, the blood pressure reading is theoretically higher than the true intra-arterial measurement.

To perform the test, one first inflates the blood pressure cuff above systolic pressure to obliterate the radial pulse. One then attempts to palpate the radial artery, a positive test is if it remains palpable as a firm "tube".

It occurs frequently in the elderly irrespective of them being hypertensive, and has moderate to modest intraobserver and interobserver agreement. It is also known as "Osler's maneuver".

The sign is named for William Osler.

The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on the person, and the risk of complications from treatment.

The diagnosis of Boerhaave's syndrome is suggested on the plain chest radiography and confirmed by chest CT scan. The initial plain chest radiograph is almost always abnormal in patients with Boerhaave's syndrome and usually reveals mediastinal or free peritoneal air as the initial radiologic manifestation. With cervical esophageal perforations, plain films of the neck show air in the soft tissues of the prevertebral space.

Hours to days later, pleural effusion(s) with or without pneumothorax, widened mediastinum, and subcutaneous emphysema are typically seen. CT scan may show esophageal wall edema and thickening, extraesophageal air, periesophageal fluid with or without gas bubbles, mediastinal widening, and air and fluid in the pleural spaces, retroperitoneum or lesser sac.

The diagnosis of esophageal perforation could also be confirmed by water-soluble contrast esophagram (Gastrografin), which reveals the location and extent of extravasation of contrast material. Although barium is superior in demonstrating small perforations, the spillage of barium sulfate into the mediastinal and pleural cavities can cause an inflammatory response and subsequent fibrosis and is therefore not used as the primary diagnostic study. If, however, the water-soluble study is negative, a barium study should be performed for better definition.

Endoscopy has no role in the diagnosis of spontaneous esophageal perforation. Both the endoscope and insufflation of air can extend the perforation and introduce air into the mediastinum.

Patients may also have a pleural effusion high in amylase (from saliva), low pH, and may contain particles of food.

Spinal arteriovenous malformations (AVMs, or angiomatous malformations) are congenital (from birth) abnormalities of blood vessels. Arteries that directly communicate with veins bypass the capillary network (which has not yet developed) and thus creates a shunt. AVMs appear as a mass of , dilated vessels. In regards to the spinal cord, they are usually located in the thoracolumbar region (between the thoracic and lumbar regions, 60% of the time), as opposed to the upper thoracic (20%) and cervical regions (approximately 15%). Cervical malformations arise from the anterior spinal artery and lie within the cord, whereas thoracolumbar malformations can be internal, external or encompass both areas of the cord.

Malformations can be recognised as part of an acute illness or gradual onset disease. In diseases such as subarachnoid hemorrhage, signs and symptoms include headache, neck stiffness and back and leg pain. Extradural, subdural and intramedullary hematomas are all signs of acute cord compression. Gradual onset diseases are more common (85-90% of all diseases leading to a diagnosis of malformation) and are usually due to an increased venous pressure. Other factors such as thrombosis or arachnoiditis can be involved. A bruit (unusual blood sounds) may be heard overlying the spinal arteriovenous malformation. Very occasionally, nevus (moles) or angiolipomas are found.

Myelography is used to confirm the diagnosis of AVMs and it shows 'snake-like' vessels on the cord's surface. If the myelogram is positive, angiography is required to show the extent of malformation and the exact site of the shunt. Magnetic resonance imaging (MRI) may show the appropriate area. If AVMs are left untreated, 50% of patients with gradual symptoms will be unable to walk within 3 years of onset. Operations can prevent progression and may improve any gait or incontinence.

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%.

Diagnosis of Harlequin syndrome is made when the individual has consistent signs and symptoms of the condition, therefore, it is made by clinical observation. In addition, a neurologist or primary care physician may require an MRI test to rule out similar disorders such as Horner's syndrome, Adie's syndrome, and Ross' syndrome. In an MRI, a radiologist may observe areas near brain or spinal cord for lesions, or any damage to the nerve endings. It is also important that the clinician rules out traumatic causes by performing autonomic function tests. Such tests includes the following: tilt table test, orthostatic blood pressure measurement, head-up test, valsalva maneuver, thermoregulatory sweat test, tendon reflex test, and electrocardiography (ECG). CT scan of the heart and lungs may also be performed to rule out a structural underlying lesion. The medical history of the individual should be carefully noted.

Thoracic insufficiency syndrome is the inability of the thorax to support normal respiration. It is frequently associated with chest and/or spinal abnormalities. Treatment options are limited, but include supportive pulmonary care and surgical options (thoracoplasty and/or implantation of vertical expandable prosthetic titanium rib (VEPTR) devices).

Mallory–Weiss syndrome often presents as an episode of vomiting up blood (hematemesis) after violent retching or vomiting, but may also be noticed as old blood in the stool (melena), and a history of retching may be absent.

In most cases, the bleeding stops spontaneously after 24–48 hours, but endoscopic or surgical treatment is sometimes required and the condition is rarely fatal.

Ultrasound remains as one of the only effective ways of prenatally diagnosing Larsen syndrome. Prenatal diagnosis is extremely important, as it can help families prepare for the arrival of an infant with several defects. Ultrasound can capture prenatal images of multiple joint dislocations, abnormal positioning of legs and knees, depressed nasal bridge, prominent forehead, and club feet. These symptoms are all associated with Larsen syndrome, so they can be used to confirm that a fetus has the disorder.

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.

Blue toe syndrome is a situation that may reflect atherothrombotic microembolism, causing transient focal ischaemia, occasionally with minor apparent tissue loss, but without diffuse forefoot ischemia. The development of blue or violaceous toes can also occur with trauma, cold-induced injury, disorders producing generalized cyanosis, decreased arterial flow, impaired venous outflow, and abnormal circulating blood.

The terms "blue toe syndrome", "grey toe syndrome" and "purple toe syndrome" are sometimes used interchangeably.

Studies may include echocardiography, thoracic and abdominal CT or MRI, peripheral arterial run off imaging studies, hypercoagulopathy labs, and interrogation of syndromes that lead to peripheral vascular pathology.

There are no diagnostic tests on which all Sneddon's patients will have abnormal results, although brain MRI and skin biopsy are often abnormal. The diagnosis is based on a detailed history and physical examination. About 40-60% of patients with the syndrome test positive for antiphospholipid antibodies.

Sneddon's patients are generally treated with warfarin, maintaining a high INR of 3-4. Because most will experience significant relief of symptoms after several months of consistent INR in this range, treatment with warfarin is often used as a diagnostic tool.

If the medical history and the actual exam of the hemangioma look typical for PHACE Syndrome, more tests are ordered to confirm the diagnosis. These tests may include:

- Ultrasound

- Magnetic resonance imaging (MRI)

- Magnetic resonance angiography of the brain (MRA)

- Echocardiogram

- Eye exam by an eye doctor

- Other tests may be needed for diagnosis and treatment