Signs and symptoms
Uvietis, Glaucoma, and Hyphema are the classic sins of UGH syndrome, but the term is often used when one, two, or all three signs are present in the presence of any IOL causing mechanical irritation of the iris or angle structures. Blurred vision, transient vision loss, eye pain, photophobia, erythropsia (objects appear red) are the main symptoms. Diagnosis
The diagnosis of UGH Syndrome is mainly based on patient history and eye examination. Patient will have history of cataract surgery with intraocular lens implantation. Slit-lamp examination may reveal hyphaema, aqueous cells and flare, iris neovascularization, mispositioned IOL, iris-lens contact, iris transillumination defects etc. Variations
UGH Plus and IPUGH (Incomplete Posterior UGH) are the variations of UGH syndrome. IPUGH is defined as bleeding into the posterior chamber with/ without glaucoma and no uveitis. UGH Plus is defined as a UGH syndrome plus a vitreous hemorrhage and occurs more frequently with anterior chamber IOLs but can occur with any IOLs. Treatment
Initially, topical and systemic medication to control inflammation and raised IOP is appropriate, but the definitive treatment is an IOL reposition or exchange. Topical corticosteroids may be used to control anterior inflammation. Raised IOP can be lowered using topical and systemic anti-glaucoma medications such as prostaglandin analogs, beta-adrenergic antagonists, alpha-adrenergic agonists, and carbonic anhydrase inhibitors etc. History
The UGH Syndrome was originally described by Ellingson in 1978 and classically included uveitis, glaucoma, and hyphaema in the setting of an anterior chamber IOL. == References ==
Monitor blood pressure response and titrate angiotensin II every 5 minutes by increments of up to 15 ng/kg/min as needed to achieve or maintain target blood pressure. Adverse effects
Angiotensin II treated patients are at an increased risk of thromboembolic events. There was a higher incidence of arterial and venous thrombotic and thromboembolic events in patients who received angiotensin II compared to placebo treated patients in the ATHOS-3 study [13% (21/163 patients) vs. 5% (8/158 patients)]. It is recommended that patients be on concurrent venous thromboembolism prophylaxis. Other adverse reactions include  thrombocytopenia, tachycardia, fungal infection, delirium, acidosis, hyperglycemia, and peripheral ischemia.Angiotensin II acts on Angiotensin receptor (AT1) on presynaptic adrenergic nerves → release of catecholamine → excessive catecholamine can be harmful as it can cause myocyte necrosis. Interactions
Angiotensin II receptor blockers, as their name implies, block the action of angiotensin II at its receptors and therefore may reduce its effects. References
External links
"Angiotensin II". Drug Information Portal. U.S. National Library of Medicine. "Angiotensin II acetate". Drug Information Portal. U.S. National Library of Medicine.