Those with ocular ischemic syndrome are typically between the ages of 50 and 80 (patients over 65) ; twice as many men as women are affected. More than 90% of those presenting with the condition have vision loss. Patients may report a dull, radiating ache over the eye and eyebrow. Those with ocular ischemic syndrome may also present with a history of other systemic diseases including arterial hypertension, diabetes mellitus, coronary artery disease, previous stroke, and hemodialysis.

The condition presents with visual loss secondary to hypoperfusion of the eye structures. The patient presents with intractable pain or ocular angina. On dilated examination, there may be blot retinal hemorrhages along with dilated and beaded retinal veins. The ocular perfusion pressure is decreased.

The corneal layers show edema and striae. There is mild anterior uveitis. A cherry-red spot may be seen in the macula, along with cotton-wool spots elsewhere, due to retinal nerve fiber layer hemorrhages. The retinal arteries may show spontaneous pulsations.

Central retinal artery occlusions cause sudden, acute, and painless loss of vision in one eye. Fundoscopic exam will show a red lesion, called a "cherry red spot," with surrounding pale retina (the pale color is caused by ischemia of the retina).

The most common cause for CRAO is carotid artery atherosclerosis. In patients of 70 years of age and older, giant cell arteritis is more likely to be the cause than in younger patients. Other causes can include dissecting aneurysms and arterial spasms.

The central retinal vein is the venous equivalent of the central retinal artery and, like that blood vessel, it can suffer from occlusion (central retinal vein occlusion, also CRVO), similar to that seen in ocular ischemic syndrome. Since the central retinal artery and vein are the sole source of blood supply and drainage for the retina, such occlusion can lead to severe damage to the retina and blindness, due to ischemia (restriction in blood supply) and edema (swelling).

It can also cause glaucoma.

Nonischemic CRVO is the milder form of the disease. It may progress to the more severe ischemic type.

Abrupt painless loss of vision in the visual field corresponding to territory of the obstructed artery is the typical history of presentation. Patients can typically define the time and extent of visual loss precisely.

Retinal whitening that corresponds to the area of ischemia is the most notable finding. In chronic phase the retinal whitening disappears.

Branch retinal artery occlusion (BRAO) is a rare retinal vascular disorder in which one of the branches of the central retinal artery is obstructed.

If carotid occlusive disease results in ophthalmic artery occlusion, general ocular ischemia may result in retinal neovascularization, rubeosis iridis, cells and flare, iris necrosis, and cataract. The condition leads to neovascularization in various eye tissues due to the ischemia. The eye pressure may become high due to associated neovascular glaucoma. An ischemic optic neuropathy may eventually occur.

Patients with BRVO usually complain of sudden onset of blurred vision or a central visual field defect.

The eye examination findings of acute BRVO include superficial hemorrhages, retinal edema, and often cotton-wool spots in a sector of retina drained by the affected vein.The obstructed vein is dilated and tortuous.

The quadrant most commonly affected is the superotemporal (63%).

Retinal neovascularization occurs in 20% of cases within the first 6–12 months of occlusion and depends on the area of retinal nonperfusion. Neovascularization is more likely to occur if more than five disc diameters of nonperfusion are present and vitreous hemorrhage can ensue.

Most patients with hypertensive retinopathy have no symptoms. However, some may report decreased or blurred vision, and headaches.

Signs of damage to the retina caused by hypertension include:

- Arteriolar changes, such as generalized arteriolar narrowing, focal arteriolar narrowing, arteriovenous nicking, changes in the arteriolar wall (arteriosclerosis) and abnormalities at points where arterioles and venules cross. Manifestations of these changes include "Copper wire arterioles" where the central light reflex occupies most of the width of the arteriole and "Silver wire arterioles" where the central light reflex occupies all of the width of the arteriole, and "arterio-venular (AV) nicking" or "AV nipping", due to venous constriction and banking.

- advanced retinopathy lesions, such as microaneurysms, blot hemorrhages and/or flame hemorrhages, ischemic changes (e.g. "cotton wool spots"), hard exudates and in severe cases swelling of the optic disc (optic disc edema), a ring of exudates around the retina called a "macular star" and visual acuity loss, typically due to macular involvement.

Mild signs of hypertensive retinopathy can be seen quite frequently in normal people (3–14% of adult individuals aged ≥40 years), even without hypertension. Hypertensive retinopathy is commonly considered a diagnostic feature of a hypertensive emergency although it is not invariably present.

Reduced blood flow to the skin layers may result in mottling or uneven, patchy discoloration of the skin

Branch retinal vein occlusion (BRVO) is a common retinal vascular disease of the elderly. It is caused by the occlusion of one of the branches of central retinal vein.

This condition is often associated with diabetes in advanced proliferative diabetic retinopathy. Other conditions causing rubeosis iridis include central retinal vein occlusion, ocular ischemic syndrome, and chronic retinal detachment.

Cardiac ischemia may be asymptomatic or may cause chest pain, known as angina pectoris. It occurs when the heart muscle, or myocardium, receives insufficient blood flow. This most frequently results from atherosclerosis, which is the long-term accumulation of cholesterol-rich plaques in the coronary arteries. Ischemic heart disease is the most common cause of death in most Western countries and a major cause of hospital admissions.

Amaurosis fugax (Latin "" meaning "fleeting", Greek "" meaning "darkening", "dark", or "obscure") is a painless temporary loss of vision in one or both eyes.

Acute limb ischaemia can occur in patients through all age groups. Patients that smoke and have diabetes mellitus are at a higher risk of developing acute limb ischaemia. Most cases involve people with atherosclerosis problems.

Symptoms of acute limb ischaemia include:

- Pain

- Pallor

- Paresthesias

- Perishingly cold

- Pulselessness

- Paralysis

These symptoms are called "the six P's'"; they are commonly mis-attributed to compartment syndrome. One more symptom would be the development of gangrene. Immediate medical attention should be sought with any of the symptoms.

In late stages, paresthesia is replaced by anesthesia due to death of nerve cells.

In some cases, gangrene can occur within six hours of ischaemia.

Many people often do not have symptoms until very late in their disease course. Patients often become symptomatic when there is irreversible damage. Symptoms are usually not painful and can include:

- Vitreous hemorrhage

- Floaters, or small objects that drift through the field of vision

- Decreased visual acuity

- "Curtain falling" over eyes

Retinal hemorrhage is a disorder of the eye in which bleeding occurs into the light sensitive tissue on the back wall of the eye. A retinal hemorrhage can be caused by hypertension, retinal vein occlusion (a blockage of a retinal vein), or diabetes mellitus (which causes small fragile blood vessels to form, which are easily damaged). Retinal hemorrhages can also occur due to shaking, particularly in young infants (shaken baby syndrome) or from severe blows to the head.

Retinal hemorrhages that take place outside the macula can go undetected for many years, and may sometimes only be picked up when the eye is examined in detail by ophthalmoscopy, fundus photography, or a dilated fundus exam. However, some retinal hemorrhages can cause severe impairment of vision. They may occur in connection with posterior vitreous detachment or retinal detachment.

The experience of amaurosis fugax is classically described as a temporary loss of vision in one or both eyes that appears as a black "curtain coming down vertically into the field of vision in one eye;" however, this altitudinal visual loss is relatively uncommon. In one study, only 23.8 percent of patients with transient monocular vision loss experienced the classic "curtain" or "shade" descending over their vision. Other descriptions of this experience include a monocular blindness, dimming, fogging, or blurring. Total or sectorial vision loss typically lasts only a few seconds, but may last minutes or even hours. Duration depends on the cause of the vision loss. Obscured vision due to papilledema may last only seconds, while a severely atherosclerotic carotid artery may be associated with a duration of one to ten minutes. Certainly, additional symptoms may be present with the amaurosis fugax, and those findings will depend on the cause of the transient monocular vision loss.

Retinopathy is any damage to the retina of the eyes, which may cause vision impairment. Retinopathy often refers to retinal vascular disease, or damage to the retina caused by abnormal blood flow. Age-related macular degeneration is technically included under the umbrella term retinopathy but is often discussed as a separate entity. Retinopathy, or retinal vascular disease, can be broadly categorized into proliferative and non-proliferative types. Frequently, retinopathy is an ocular manifestation of systemic disease as seen in diabetes or hypertension. Diabetes is the most common cause of retinopathy in the U.S. as of 2008. Diabetic retinopathy is the leading cause of blindness in working-aged people. It accounts for about 5% of blindness worldwide and is designated a priority eye disease by the World Health Organization.

Acute limb ischaemia (ALI) occurs when there is a sudden lack of blood flow to a limb.

Acute limb ischaemia is caused by embolism or thrombosis, or rarely by dissection or trauma. Thrombosis is usually caused by peripheral vascular disease (atherosclerotic disease that leads to blood vessel blockage), while an embolism is usually of cardiac origin. In the United States, ALI is estimated to occur in 14 out of every 100,000 people per year. With proper surgical care, acute limb ischaemia is a highly treatable condition; however, delayed treatment (beyond 6 to 12 hours) can result in permanent disability, amputation, and/or death.

The New Latin term "ischaemia" as written, is a British version of the word "ischemia", and stems from the Greek terms "ischein" 'to hold'; and "haima" 'blood'. In this sense, ischaemia refers to the inhibition of blood flow to/through the limb.

Symptoms may begin quickly or slowly depending on the size of the embolus and how much it blocks the blood flow. Symptoms of embolisation in an organ vary with the organ involved but commonly include:

- Pain in the involved body part

- Temporarily decreased organ function

Later symptoms are closely related to infarction of the affected tissue. This may cause permanently decreased organ function.

For example, symptoms of myocardial infarction mainly include chest pain, dyspnea, diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations.

Symptoms of limb infarction include coldness, decreased or no pulse beyond the site of blockage, pain, muscle spasm, numbness and tingling, pallor and muscle weakness, possibly to the grade of paralysis in the affected limb.

Retinal haemorrhages commonly occur in high attitude climbers, most likely due to the effects of systemic hypoxia on the eye. Risk is correlated with the maximum altitude reached, duration of exposure to high altitude conditions, and climb rate.

Thrombotic Storm has been seen in individuals of all ages and races. The initial symptoms of TS present in a similar fashion to the symptoms experienced in deep vein thrombosis. Symptoms of a DVT may include pain, swelling and discoloration of the skin in the affected area. As with DVTs patients with TS may subsequently develop pulmonary emboli. Although the presentation of TS and DVTs are similar, TS typically progresses rapidly, with numerous clots occurring within a short period of time. After the formation of the initial clot a patient with TS typically begins a “clotting storm” with the development of multiple clots throughout the body. Rapid progression within a short period of time is often seen, affecting multiple organs systems. The location of the clot is often unusual or found in a spot in the body that is uncommon such as the dural sinus. Patients tend to respond very well to anticoagulation such as coumadin or low molecular weight heparin but may become symptomatic when treatment is withheld.

While the key clinical characteristics of thrombotic storm are still being investigated, it is believed that the clinical course is triggered by a preexisting condition, known as a hypercoagulable state. These can include such things as pregnancy, trauma or surgery. Hypercoagulable states can be an inherited or acquired risk factor that then serves as a trigger to initiate clot formation. However, in a subset of patient with TS a trigger cannot be identified. Typically people with TS will have no personal or family history of coagulations disorders.

Arterial emboli often occur in the legs and feet. Some may occur in the brain, causing a stroke, or in the heart, causing a heart attack. Less common sites include the kidneys, intestines, and eyes.