In order to treat acute limb ischaemia there are a series of things that can be done to determine where the occlusion is located, the severity, and what the cause was. To find out where the occlusion is located one of the things that can be done is simply a pulse examination to see where the heart rate can be detected and where it stops being sensed. Also there is a lower body temperature below the occlusion as well as paleness. A Doppler evaluation is used to show the extent and severity of the ischaemia by showing flow in smaller arteries. Other diagnostical tools are duplex ultrasonography, computed tomography angiography (CTA), and magnetic resonance angiography (MRA). The CTA and MRA are used most often because the duplex ultrasonography although non-invasive is not precise in planning revascularization. CTA uses radiation and may not pick up on vessels for revascularization that are distal to the occlusion, but it is much quicker than MRA. In treating acute limb ischaemia time is everything.

In the worst cases acute limb ischaemia progresses to critical limb ischaemia, and results in death or limb loss. Early detection and steps towards fixing the problem with limb-sparing techniques can salvage the limb. Compartment syndrome can occur because of acute limb ischaemia because of the biotoxins that accumulate distal to the occlusion resulting in edema.

As the cause of the ischemia can be due to embolic or thrombotic occlusion of the mesenteric vessels or nonocclusive ischemia, the best way to differentiate between the etiologies is through the use of mesenteric angiography. Though it has serious risks, angiography provides the possibility of direct infusion of vasodilators in the setting of nonocclusive ischemia.

A number of devices have been used to assess the sufficiency of oxygen delivery to the colon. The earliest devices were based on tonometry, and required time to equilibrate and estimate the pHi, roughly an estimate of local CO levels. The first device approved by the U.S. FDA (in 2004) used visible light spectroscopy to analyze capillary oxygen levels. Use during aortic aneurysm repair detected when colon oxygen levels fell below sustainable levels, allowing real-time repair. In several studies, specificity has been 83% for chronic mesenteric ischemia and 90% or higher for acute colonic ischemia, with a sensitivity of 71%-92%. This device must be placed using endoscopy, however.

The major cause of acute limb ischaemia is arterial thrombosis (85%), while embolic occlusion is responsible for 15% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a thrombosis or embolism resulting in ischaemia.

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

The differentiating presentations are suggestive of FMD being a unique syndrome in respect to the pediatric population. Experienced FMD clinicians warn against relying in the “string of beads” angiography for a diagnosis. In fact, it is suggested that FMD may be both under and over-diagnosed in children with stroke.

It is the lack of specific symptoms and its potential to appear anywhere that makes FMD a challenge to detect early on. The most accurate diagnosis comes from combining clinical presentation and angiographic imaging. According to the Michigan Outcomes Research and Reporting Program (MCORRP, 2013) the length of time from a patient’s first signs or symptoms to diagnosis is commonly 5 years.

FMD is currently diagnosed through the use of both invasive and non-invasive tests. Non-invasive testing includes duplex ultrasonography, magnetic resonance angiography (MRA), and computed tomographic angiography (CTA). Invasive testing through angiography is the gold standard. However, due to the higher risk of complications this is typically not done early on. Occasionally, FMD is diagnosed asymptomatically after an unrelated x-ray presents the classic ‘string of beads’ appearance of the arteries, or when a practitioner investigates an unexpected bruit found during an exam. When a diagnosis of FMD is considered for a patient thorough medical history, family history as well as vascular examination should be completed.

A definitive diagnosis of FMD can only be made with imaging studies. Catheter-based angiography (with contrast) has proven to be the most accurate imaging technique: this test involves a catheter is inserted into a large artery and advanced until it reaches the vessel of question. The catheter allows practitioners to view and measure the pressure of the artery aiding in the categorization and severity of the FMD diseased artery. According to Olin, “catheter-based angiography is the only imaging modality that can accurately identify the changes of FMD, aneurysm formation, and dissection in the branch vessels.” Practitioners believe it is important to utilize IVUS imaging because stenosis can sometimes only be detected through the methods of pressure gradient or IVUS imaging. In addition, computed tomography angiography and magnetic resonance angiography are commonly used to evaluate arteries in the brain. Doppler ultrasound may be used in both the diagnosis and follow-up of FMD.

Smith (2015) conducted a study that looked into specific biological markers that correlate to Moyamoya disease. Some of the categories of these biomarkers include phenotypes - conditions commonly related to Moyamoya, radiographical markers for the diagnosis of Moyamoya, and proteins as well as cellular changes that occur in cases of Moyamoya.

Similar to Moyamoya Disease, there are conditions that are closely associated with Moyamoya Syndrome. Some of the more common medical conditions that are closely associated with Moyamoya Syndrome include trisomy 21 (Down's Syndrome), sickle cell disease, and neurofibromatosis type 1. There is also evidence that identifies hyperthyroidism and congenital dwarfing syndromes as two of the more loosely associated syndromes that correlate with the possibility of being diagnosed with Moyamoya Disease later in life.

There is also research that has shown that certain radiographic biomarkers that lead to the diagnosis of Moyamoya Disease have been identified. The specific radiographic markers are now considered an acceptable key component to Moyamoya Disease and have been added to the INternational Classification of Diseases (ICD). These biomarkers of Moyamoya are "stenosis of the distal ICA's up to and including the bifurcation, along with segments of the proximal ACA and MCA...dilated basal collateral vessels must be present" Some other common findings that have not been added to the classification index of those with Moyamoya Disease which are found using radiography involve very distinct changes in the vessels of the brain. These changes include newly formed vessels made to compensate for another change noted, ischemia and cerebrovascular reserve, both found on MRI. Functional changes include evidence of ischemia in vessels of the brain (ICA, ACA, MCA, specifically). It is important to also note that the radiographic biomarkers, in order to be classified as Moyamoya Disease, all findings must be bilateral. If this is not the case and the findings are unilateral, it is diagnosed as Moyamoya Syndrome.

There are also several protein biomarkers that have been linked to the Moyamoya Disease diagnosis. Although the sample size of the studies performed are small due to the rarity of the disease, the findings are indicative of a correlation between the disease and several specific protein biomarkers. Other studies have confirmed the correlation of Moyamoya and adhesion molecule 1 (ICAM-1) being increased as compared to normal vascular function counterparts Furthermore, it has been concluded that the localization of inflammatory cells suggests that the inflammation stimulus iteself may be responsible for the proliferation and occlusion in the ICA, ACA, and MCA found in those with Moyamoya Disease.

The gold standard for measuring endothelial function is angiography with acetylcholine injection. Previously, this was not done outside of research because of the invasive and complex nature of the procedure. As mentioned above, the use of acetylcholine injections to test vasodilation is now safely used for procedures where arterial catheterization is employed (this method is less frequently used though, so overall acetylcholine is not used very often in this way).

A noninvasive method to measure endothelial dysfunction is % Flow Mediated Dilation (FMD) as measured by Brachial Artery Ultrasound Imaging (BAUI). Current measurements of endothelial function via FMD vary due to technical and physiological factors. For example, FMD is largely affected by hormones, especially for women. FMD values can differ for the same woman if she is in different phases of her menstrual cycle during the time of measurement. When using this technique on people who suffer from things like heart failure, renal failure, or hypertension, their increased sympathetic tone can often falsify the results. Furthermore, a negative correlation between percent flow mediated dilation and baseline artery size is recognised as a fundamental scaling problem, leading to biased estimates of endothelial function. For research on FMD an ANCOVA approach to adjusting FMD for variation in baseline diameter is more appropriate. Another challenge of FMD is variability across centers and the requirement of highly qualified technicians to perform the procedure.

A non-invasive, FDA-approved device for measuring endothelial function that works by measuring Reactive Hyperemia Index (RHI) is Itamar Medical's EndoPAT™. It has shown an 80% sensitivity and 86% specificity to diagnose coronary artery disease when compared against the gold standard, acetylcholine angiogram. This results suggests that this peripheral test reflects the physiology of the coronary endothelium. Endopat has been tested in several clinical trials at multiple centers (including major cohort studies such as the Framingham Heart Study, the Heart SCORE study, and the Gutenberg Health Study). The results from clinical trials have shown that EndoPAT™ is useful for risk evaluation, stratification and prognosis of getting major cardiovascular events (MACE).

Since NO maintains low tone and high compliance of the small arteries at rest a reduction of age-dependent small artery compliance is a marker for endothelial dysfunction that is associated with both functional and structural changes in the microcirculation that are predictive of subsequent morbid events Small artery compliance or stiffness can be assessed simply and at rest and can be distinguished from large artery stiffness by use of pulsewave analysis with the CV Profilor.

The diagnosis of moyamoya is suggested by CT, MRI, or angiogram results. Contrast-enhanced T1-weighted images are better than FLAIR images for depicting the leptomeningeal ivy sign in moyamoya disease. MRI and MRA should be performed for the diagnosis and follow-up of moyamoya disease. Diffusion-weighted imaging can also be used for following the clinical course of children with moyamoya disease, in whom new focal deficits are highly suspicious of new infarcts.

Proliferation of smooth muscle cells in the walls of the Moyamoya affected arteries has been found to be representative of the disease. A study of six autopsies of six patients who died from Moyamoya disease lead to the finding that there is evidence that supports the theory that there is a thickening, or proliferation, of the innermost layer of the vessels affected by Moyamoya. These vessels are the ACA (anterior cerebral artery), MCA (middle cerebral artery), and ICA (internal carotid artery). The occlusion of the ICA results in concomitant diminution of the "puff-of-smoke" collaterals, as they are supplied by the ICA.

Often nuclear medicine studies such as SPECT (single photon emission computerized tomography) are used to demonstrate the decreased blood and oxygen supply to areas of the brain involved with moyamoya disease. Conventional angiography provided the conclusive diagnosis of moyamoya disease in most cases and should be performed before any surgical considerations.

Dr. Darren B. Orbach, MD, PhD explains how the disease progresses as well as the role angiography plays in detecting the progression of Moyamoya in a short video

Non-occlusive disease has a poor prognosis with survival rate between 40-50%.

Diagnosis is based on the demonstration of vascular lesions in large and middle-sized vessels on angiography, CT scan, magnetic resonance angiography or FDG PET. FDG PET can help in diagnosis of active inflammation not just in patients with active Takayasu arteritis prior to treatment but also in addition in relapsing patients receiving immunosuppressive agents.

Contrast angiography has been the gold standard. The earliest detectable lesion is a local narrowing or irregularity of the lumen. This may develop into stenosis and occlusion. The characteristic finding is the presence of "skip lesions," where stenosis or aneurysms alternate with normal vessels. Angiography provides information on vessel anatomy and patency but does not provide information on the degree of inflammation in the wall.

The age at onset helps to differentiate Takayasu's arteritis from other types of large vessel vasculitis. For example, Takaysu's arteritis has an age of onset of 60 years.

Takayasu arteritis is not associated with ANCA, rheumatoid factor, ANA, and anticardiolipin antibodies.

CT angiography would be helpful in differentiating occlusive from non-occlusive causes of mesenteric ischaemia.

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

Ancillary testing is not usually necessary to make the diagnosis. Fluorescein angiography reveals an abrupt diminution in dye at the site of the obstruction. Visual field testing can confirm the extent of visual loss.

Currently laboratory testing is not as reliable as observation when it comes to defining the parameters of Thrombotic Storm. Careful evaluation of possible thrombosis in other organ systems is pertinent in expediting treatment to prevent fatality.Preliminary diagnosis consists of evidence documented with proper imaging studies such as CT scan, MRI, or echocardiography, which demonstrate a thromboembolic occlusion in the veins and/or arteries. Vascular occlusions mentioned must include at least two of the clinic events:

- Deep venous thrombosis affecting one (or more) limbs and/or pulmonary embolism.

- Cerebral vein thrombosis.

- Portal vein thrombosis, hepatic vein, or other intra-abdominal thrombotic events.

- Jugular vein thrombosis in the absence of ipsilateral arm vein thrombosis and in the absence of ipsilateral central venous access.

- Peripheral arterial occlusions, in the absence of underlying atherosclerotic vascular disease,

- resulting in extremity ischemia and/or infarction.

- Myocardial infarction, in the absence of severe coronary artery disease

- Stroke and/or transient ischemic attack, in the absence of severe atherosclerotic disease and at an age less than 60 years.

- Central retinal vein and/or central retinal arterial thrombosis.

- Small vessel thrombosis affecting one or more organs, systems, or tissue; must be documented by histopathology.

In addition to the previously noted vascular occlusions, development of different thromboembolic manifestations simultaneously or within one or two weeks must occur and the patient must have an underlying inherited or acquired hypercoagulable state (other than Antiphospholipid syndrome)

This is based on MRI scan, magnetic resonance angiography and CT scan. A cerebral digital subtraction angiography (DSA) enhances visualization of the fistula.

- CT scans classically show an enlarged superior ophthalmic vein, cavernous sinus enlargement ipsilateral (same side) as the abnormality and possibly diffuse enlargement of all the extraocular muscles resulting from venous engorgement.

- Selective arteriography is used to evaluate arteriovenous fistulas.

- High resolution digital subtraction angiography may help in classifying CCF into dural and direct type and thus formulate a strategy to treat it either by a balloon or coil or both with or without preservation of parent ipsilateral carotid artery.

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.

Vascular occlusion is a blockage of a blood vessel, usually with a clot. It differs from thrombosis in that it can be used to describe any form of blockage, not just one formed by a clot. When it occurs in a major vein, it can, in some cases, cause deep vein thrombosis. The condition is also relatively common in the retina, and can cause partial or total loss of vision. An occlusion can often be diagnosed using Doppler sonography (a form of ultrasound).

Some medical procedures, such as embolisation, involve occluding a blood vessel to treat a particular condition. This can be to reduce pressure on aneurysms (weakened blood vessels) or to restrict a haemorrhage. It can also be used to reduce blood supply to tumours or growths in the body, and therefore restrict their development. Occlusion can be carried out using a ligature; by implanting small coils which stimulate the formation of clots; or, particularly in the case of cerebral aneurysms, by clipping.

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.

Nutcracker syndrome can be diagnosed with:

- Left renal venography—considered to be the gold standard test.

- Computed tomography (CT).

- Abdominal ultrasonography—not definitive but has been found to be useful.

Stent implantation has been correlated with impaired endothelial function in several studies. According to Mischie et al., sirolimus eluting stent implantation induces a higher rate of endothelial dysfunction compared to bare metal stents. This is problematic because stents have been used to treat many diseases related to endothelial dysfunction, including coronary artery disease. Sirolimus eluting stents were previously used because they showed very low rates of in-stent restenosis but further investigation showed that they often impair endothelial dysfunction in humans and worsen conditions. Therefore, now the commonly used drug is iopromide-paclitaxel because it showed low rates of in-stent restenosis and thrombosis and it does not worsen the person's health condition.

No proved treatment exists for branch retinal artery occlusion.

In the rare patient who has branch retinal artery obstruction accompanied by a systemic disorder, systemic anti-coagulation may prevent further events.

There is a recent optical test, but it requires endoscopy (see Diagnosis). There are no specific blood tests for ischemic colitis. The sensitivity of tests among 73 patients were:

- The white blood cell count was more than 15,000/mm3 in 20 patients (27%)

- The serum bicarbonate level was less than 24 mmol/L in 26 patients (36%)

Plain X-rays are often normal or show non-specific findings. In a series of 73 patients, plain abdominal radiography (56%) showing colic distension in 53% or a pneumoperitoneum in 3%.

CT scans are often used in the evaluation of abdominal pain and rectal bleeding, and may suggest the diagnosis of ischemic colitis, pick up complications, or suggest an alternate diagnosis.

Endoscopic evaluation, via colonoscopy or flexible sigmoidoscopy, is the procedure of choice if the diagnosis remains unclear. Ischemic colitis has a distinctive endoscopic appearance; endoscopy can also facilitate alternate diagnoses such as infection or inflammatory bowel disease. Biopsies can be taken via endoscopy to provide more information. Visible light spectroscopy, performed using catheters placed through the 5 mm channel of the endoscope, is diagnostic (see Diagnosis).

Diagnosis of cerebrovascular disease is done by (among other diagnoses):

- clinical history

- physical exam

- neurological examination.

It is important to differentiate the symptoms caused by a stroke from those caused by syncope (fainting) which is also a reduction in cerebral blood flow, almost always generalized, but they are usually caused by systemic hypotension of various origins: cardiac arrhythmias, myocardial infarction, hemorrhagic shock, among others.