The monocytes differentiate into macrophages, which proliferate locally, ingest oxidized LDL, slowly turning into large "foam cells" – so-called because of their changed appearance resulting from the numerous internal cytoplasmic vesicles and resulting high lipid content. Under the microscope, the lesion now appears as a fatty streak. Foam cells eventually die and further propagate the inflammatory process.In addition to these cellular activities, there is also smooth muscle proliferation and migration from the tunica media into the intima in response to cytokines secreted by damaged endothelial cells. This causes the formation of a fibrous capsule covering the fatty streak. Intact endothelium can prevent this smooth muscle proliferation by releasing nitric oxide. Calcification and lipids
Calcification forms among vascular smooth muscle cells of the surrounding muscular layer, specifically in the muscle cells adjacent to atheromas and on the surface of atheroma plaques and tissue. In time, as cells die, this leads to extracellular calcium deposits between the muscular wall and outer portion of the atheromatous plaques. With the atheromatous plaque interfering with the regulation of the calcium deposition, it accumulates and crystallizes. A similar form of intramural calcification, presenting the picture of an early phase of arteriosclerosis, appears to be induced by many drugs that have an antiproliferative mechanism of action (Rainer Liedtke 2008).Cholesterol is delivered into the vessel wall by cholesterol-containing low-density lipoprotein (LDL) particles. To attract and stimulate macrophages, the cholesterol must be released from the LDL particles and oxidized, a key step in the ongoing inflammatory process.
There is little evidence that most of the commonly used treatments for hyphema (antifibrinolytic agents [oral and systemic aminocaproic acid, tranexamic acid, and aminomethylbenzoic acid], corticosteroids [systemic and topical], cycloplegics, miotics, aspirin, conjugated estrogens, traditional Chinese medicine, monocular versus bilateral patching, elevation of the head, and bed rest) are effective at improving visual acuity after two weeks. Surgery may be necessary for non-resolving hyphemas, or hyphemas that are associated with high pressure that does not respond to medication. Surgery can be effective for cleaning out the anterior chamber and preventing corneal blood staining.If pain management is necessary, acetaminophen can be used. Aspirin and ibuprofen should be avoided, because they interfere with platelets ability to form a clot and consequently increase the risk of additional bleeding. Sedation is not usually necessary for patients with hyphema. Aminocaproic or tranexamic acids are often prescribed for hyphema on the basis that they reduce the risk of rebleeding by inhibiting the conversion of plasminogen to plasmin, and thereby keeping clots stable. However, the evidence for their effectiveness is limited and aminocaproic acid may actually cause hyphemas to take longer to clear. Prognosis
Hyphemas require urgent assessment by an optometrist or ophthalmologist as they may result in permanent visual impairment.A long-standing hyphema may result in hemosiderosis and heterochromia. Blood accumulation may also cause an elevation of the intraocular pressure. On average, the increased pressure in the eye remains for six days before dropping. Most uncomplicated hyphemas resolve within 5–6 days.