The lesion can be easily identified clinically. Arterial doppler and pulse volume recordings are performed for baseline assessment of blood flow. Radiographs may be necessary to rule out osteomyelitis.

The microscopic examination of tissue (histology) gives the definitive diagnosis. The diagnostic histopathologic finding is intravascular cholesterol crystals, which are seen as cholesterol clefts in routinely processed tissue (embedded in paraffin wax). The cholesterol crystals may be associated with macrophages, including giant cells, and eosinophils.

The sensitivity of small core biopsies is modest, due to sampling error, as the process is often patchy. Affected organs show the characteristic histologic changes in 50-75% of the clinically diagnosed cases. Non-specific tissue findings suggestive of a cholesterol embolization include ischemic changes, necrosis and unstable-appearing complex atherosclerotic plaques (that are cholesterol-laden and have a thin fibrous cap). While biopsy findings may not be diagnostic, they have significant value, as they help exclude alternate diagnoses, e.g. vasculitis, that often cannot be made confidently based on clinical criteria.

Tests for inflammation (C-reactive protein and the erythrocyte sedimentation rate) are typically elevated, and abnormal liver enzymes may be seen. If the kidneys are involved, tests of renal function (such as urea and creatinine) are elevated. The complete blood count may show particularly high numbers of a type of white blood cell known as "eosinophils" (more than 0.5 billion per liter); this occurs in only 60-80% of cases, so normal eosinophil counts do not rule out the diagnosis. Examination of the urine may show red blood cells (occasionally in casts as seen under the microscope) and increased levels of protein; in a third of the cases with kidney involvement, eosinophils can also be detected in the urine. If vasculitis is suspected, complement levels may be determined as reduced levels are often encountered in vasculitis; complement is a group of proteins that forms part of the innate immune system. Complement levels are frequently reduced in cholesterol embolism, limiting the use of this test in the distinction between vasculitis and cholesterol embolism.

Since the cause of FAD has not been genetically pinpointed, the only way to diagnose FAD is through the examination of phenotypic variations in the aorta. Usually echocardiography is used to take measurements of the aortic root as well as transesophageal echocardiography. Biomarkers lend a quick way to diagnose dissection when time is of the essence. These have the ability to relay the levels of smooth muscle mysosin heavy chain protein present, which is released from damaged aortic tissue.

There are two types of FAD; groups A and B. Normally if any area of the ascending aorta is involved in the dissection this is considered group A. If the dissection occurs within the descending aorta this is classified in group B. These two groups can than be broken down into three classes of FAD: Type 1, Type 2 and Type 3. Group A consists of Types 1 and 2, whereas Group B consists only of Type 3. Type 1 encompasses dissection in the distal ascending aorta closest to the heart, not including the aortic arch. Type 2 refers to dissection of the ascending aorta, closer to and including the aortic arch. Type 3 refers to the descending thoracic and abdominal aorta.

Group A dissections are the more serious of the two due to the location of the dissection in the ascending aorta, which leads to a higher risk of congestive heart failure and pericardium and/or aortic valve rupture. Individuals also tend to be predisposed to type A if they do have Marfans or Elhers-Danlos syndromes. These contribute to a higher fatality rate in group A dissection if immediate surgery is not performed. The most common corrective surgeries are actual aortic valve replacement and coronary artery bypass. The five year survival rate after surgery is a successful 70.4% due to vigilant monthly physical exams and chest x-rays to monitor progress. Group B dissections typically have a higher surgery mortality rate and are therefore not good candidates. Instead medical management is the common response to treating and keeping dissections of the descending aorta under control.

A selective coronary angiogram is the most common method to diagnose the condition, although it is sometimes not recognised until after death. Intravascular ultrasound (IVUS) is also used as it is able to more easily differentiate the condition from atherosclerotic disease.

Treatment is varied depending upon the nature of the case. In severe cases, coronary artery bypass surgery is performed to redirect blood flow around the affected area. Drug-eluting stents and thrombolytic drug therapy are less invasive options for less severe cases.

Complications such as rupture or other life-threatening conditions are rare. Treatment may involve surgery, particularly when signs indicating worsening are present (the patient is unable to control their pain or changes in blood pressure).

The prevalence of arterial insufficiency ulcers among people with Diabetes is high due to decreased blood flow caused by the thinning of arteries and the lack of sensation due to diabetic neuropathy. Prevention is the first step in avoiding the development of an arterial insufficiency ulcer. These steps could include annual podiatry check ups that include, "assessment of skin, checking of pedal pulses (assessing for blood flow) and assessing physical sensation".

The management of arterial insufficiency ulcers depends on the severity of the underlying arterial insufficiency. The affected region can sometimes be revascularized via vascular bypass or angioplasty. If infection is present, appropriate antibiotics are prescribed. When proper blood flow is established, debridement is performed. If the wound is plantar (on walking surface of foot), patient is advised to give rest to foot to avoid enlargement of the ulcer. Proper glycemic control in diabetics is important. Smoking should be avoided to aid wound healing.

Currently, there is controversy over whether or not inheritance truly plays a role in FAD, and if so which gene it acts upon. FAD does not come from strictly one predisposing factor, such as hypertension. It is suggested that the combination of environmental factors along with genetics may contribute to causing FAD. Before newer and more effective cures and therapies can be developed, first the specific gene mutation must be identified. Until such a gene is determined, scientists say patient education, and physician awareness is vital. Currently scientists have found animal models to be beneficial in understanding the pathology behind FAD. In the future there is hope to develop drugs that will better support and strengthen the aortic wall. Endovascular methods of treatment are becoming increasingly popular, and scientists hope to use this technique in both acute and chronic cases.

The condition is often associated with thickening of the aortic wall, and can be differentiated from similar conditions (atherosclerotic plaque and a thrombus) through the use of computed tomography and magnetic resonance imaging, though the latter is superior. Transesophageal echocardiography and intravascular ultrasonography may also be used in differentiation.

A clinical severity score has been developed to assess chronic venous ulcers. It is based on the CEAP (clinical, etiology, anatomy, and pathophysiology) classification system developed by an expert panel. A high score gives a poor prognosis.

Unstable angina is characterized by at least one of the following:

1. Occurs at rest or minimal exertion and usually lasts more than 20 minutes (if nitroglycerin is not administered)

2. Being severe (at least Canadian Cardiovascular Society Classification 3) and of new onset (i.e. within 1 month)

3. Occurs with a crescendo pattern (brought on by less activity, more severe, more prolonged or increased frequency than previously).

Fifty percent of people with unstable angina will have evidence of necrosis of the heart's muscular cells based on elevated cardiac serum markers such as creatine kinase isoenzyme (CK)-MB and troponin T or I, and thus have a diagnosis of non-ST elevation myocardial infarction.

Compression stockings appear to prevent the formation of new ulcers in people with a history of venous ulcers.

Nitroglycerin can be used immediately to widen the coronary arteries and help increase blood flow to the heart. In addition, nitroglycerin causes peripheral venous and artery dilation reducing cardiac preload and afterload. These reductions allow for decreased stress on the heart and therefore lower the oxygen demand of the heart's muscle cells.

Antiplatelet drugs such as aspirin and clopidogrel can help reduce the progression of atherosclerotic plaque formation, as well as combining these with an anticoagulant such as a low molecular weight heparin.

Areas of severe narrowing, stenosis, detectable by angiography, and to a lesser extent "stress testing" have long been the focus of human diagnostic techniques for cardiovascular disease, in general. However, these methods focus on detecting only severe narrowing, not the underlying atherosclerosis disease. As demonstrated by human clinical studies, most severe events occur in locations with heavy plaque, yet little or no lumen narrowing present before debilitating events suddenly occur. Plaque rupture can lead to artery lumen occlusion within seconds to minutes, and potential permanent debility and sometimes sudden death.

Plaques that have ruptured are called complicated plaques. The extracellular matrix of the lesion breaks, usually at the shoulder of the fibrous cap that separates the lesion from the arterial lumen, where the exposed thrombogenic components of the plaque, mainly collagen will trigger thrombus formation. The thrombus then travels downstream to other blood vessels, where the blood clot may partially or completely block blood flow. If the blood flow is completely blocked, cell deaths occur due to the lack of oxygen supply to nearby cells, resulting in necrosis. The narrowing or obstruction of blood flow can occur in any artery within the body. Obstruction of arteries supplying the heart muscle results in a heart attack, while the obstruction of arteries supplying the brain results in a stroke.

Lumen stenosis that is greater than 75% was considered the hallmark of clinically significant disease in the past because recurring episodes of angina and abnormalities in stress tests are only detectable at that particular severity of stenosis.

However, clinical trials have shown that only about 14% of clinically debilitating events occur at sites with more than 75% stenosis. The majority of cardiovascular events that involve sudden rupture of the atheroma plaque do not display any evident narrowing of the lumen.

Thus, greater attention has been focused on "vulnerable plaque" from the late 1990s onwards.

Besides the traditional diagnostic methods such as angiography and stress-testing, other detection techniques have been developed in the past decades for earlier detection of atherosclerotic disease. Some of the detection approaches include anatomical detection and physiologic measurement.

Examples of anatomical detection methods include coronary calcium scoring by CT, carotid IMT (intimal media thickness) measurement by ultrasound, and intravascular ultrasound (IVUS). Examples of physiologic measurement methods include lipoprotein subclass analysis, HbA1c, hs-CRP, and homocysteine.

Both anatomic and physiologic methods allow early detection before symptoms show up, disease staging and tracking of disease progression. Anatomic methods are more expensive and some of them are invasive in nature, such as IVUS. On the other hand, physiologic methods are often less expensive and safer. But they do not quantify the current state of the disease or directly track progression. In recent years, developments in nuclear imaging techniques such as PET and SPECT have provided ways of estimating the severity of atherosclerotic plaques.

Diabetics, despite not having clinically detectable atherosclerotic disease, have more severe debility from atherosclerotic events over time than non-diabetics who have already had atherosclerotic events. Thus diabetes has been upgraded to be viewed as an advanced atherosclerotic disease equivalent.

Steps to prevent diabetic foot ulcers include frequent review by a foot specialist, good foot hygiene, diabetic socks and shoes, as well as avoiding injury.

- Foot-care education combined with increased surveillance can reduce the incidence of serious foot lesions.

Stress ulcer is suspected when there is upper gastrointestinal bleeding in the appropriate clinical setting, for example, when there is upper gastrointestinal bleeding in elderly patients in a surgical intensive care unit (ICU) with heart and lung disease, or when there is upper gastrointestinal bleeding in patients in a medical ICU who require respirators.

Stress ulcer can be diagnosed after the initial management of gastrointestinal bleeding, the diagnosis can be confirmed by upper GI endoscopy.

In the United Kingdom, the Royal College of Nursing has published guidelines in 'Pressure ulcer risk assessment and prevention' that call for identifying people at risk and taking preventative action; the UK National Standards for Care Homes (UK) to do so as well.

Internationally, the NPUAP, EPUAP and Pan Pacific Pressure Injury Alliance (Australia, New Zealand, Singapore and Hong Kong) published comprehensive evidence-based clinical practice guidelines in 2014. The guideline was developed by an international team of over 100 clinical specialists and updates the 2009 EPUAP and NPUAP clinical guidelines. The guideline includes recommendations on strategies to prevent pressure ulcers including the use of pressure redistributing support surfaces, repositioning and maintaining appropriate nutritional support.

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)

The prevalence of Mönckeberg's arteriosclerosis increases with age and is more frequent in diabetes mellitus, chronic kidney disease, systemic lupus erythematosus, chronic inflammatory conditions, hypervitaminosis D and rare genetic disorders, such as Keutel syndrome. The prevalence of Monckeberg's arteriosclerosis in the general population has been estimated as 1.5; however the validity of this criterion is questionable.

In addition, adequate intake of protein and calories is important. vitamin C has been shown to reduce the risk of pressure ulcers. People with higher intakes of vitamin C have a lower frequency of bed sores in those who are bedridden than those with lower intakes. Maintaining proper nutrition in newborns is also important in preventing pressure ulcers. If unable to maintain proper nutrition through protein and calorie intake, it is advised to use supplements to support the proper nutrition levels. Skin care is also important because damaged skin does not tolerate pressure. However, skin that is damaged by exposure to urine or stool is not considered a pressure ulcer. These skin wounds should be classified as Incontinence Associated Dermatitis.

The evidence for special footwear to prevent foot ulcers is poor.

"Clinical Evidence" reviewed the topic and concluded "Individuals with significant foot deformities should be considered for referral and assessment for customised shoes that can accommodate the altered foot anatomy. In the absence of significant deformities, high quality well fitting non-prescription footwear seems to be a reasonable option". National Institute for Health and Clinical Excellence concluded that for people at "high risk of foot ulcers (neuropathy or absent pulses plus deformity or skin changes or previous ulcer" that "specialist footwear and insoles" should be provided.

People with loss of feeling in their feet should inspect their feet on a daily basis, to ensure that there are no wounds starting to develop. They should not walk around barefoot, but use proper footwear at all times.

Some of the investigations done for ulcer are:

- Study of discharging fluid: Culture and sensitivity

- Edge biopsy: Edge contains multiplying cells

- Radiograph of affected area to look for periostitis or osteomyelitis

- FNAC of lymph node

- Chest X-ray and Mantoux test in suspected tuberculous ulcer

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.