Jenna Williams, OD - Ocular Disease Resident, Battle Creek VAMC

I. CASE HISTORY - Patient demographics: 65 year old white male - Chief complaint: Constant, blurry, painful OS for 4 months - Ocular history: Pseudophakia OU, s/p YAG capsulotomy OD, of prematurity OU - Medical history: Hypertension - Medications: Amlodipine - Other salient information: Last eye exam was 4 months ago for 1 month CE post-op OS, surgical notes indicated CE OS was long in duration, but no complications were noted

II. PERTINENT FINDINGS Entrance testing: - Entering corrected visual acuities : 20/50, PH 20/25 OD, 20/60, PH NI OS - All preliminary findings and testing were normal Anterior slit lamp examination: - OD: CCI, PCIOL, otherwise unremarkable - OS: CCI, trace corneal endothelial pigment, 1+ diffuse conjunctival injection, 1+ mixed cells in anterior chamber, inferior transillumination defects, PCIOL Applanation tonometry: 12mmHg OD, 11mmHg OS Posterior segment OU: C/D 0.25r, Vitreous clear, ONH pink, distinct margins, Macula clear Other testing: - 40mHz B-scan Ultrasonography, OS: single-piece IOL in capsular bag, nasally decentered with an inferior-temporal tilt and in contact with posterior iris surface along inferior pupillary margin, haptics positioned along vertical plane and in contact with ciliary process and inferior posterior iris.

III. DIFFERENTIAL DIAGNOSES - Hyphema (UGH) Syndrome - Retained fragment - Chronic postoperative

IV. DIAGNOSIS Primary Diagnosis: Uveitis Hyphema Glaucoma Syndrome, OS - Etiology confirmed on B-scan Ultrasonography and Ann Arbor VA concurred on consultation.

V. TREATMENT and MANAGEMENT - The patient was instructed to begin using prednisolone acetate 1% QID OS and ketorolac 0.5% QID OS while awaiting surgical referral with ophthalmology. IOL repositioning surgery was soon scheduled and performed without complication. - On post-op day six, the patient presented at the BCVAMC for an urgent care visit with a sudden onset of severe pain and decreased vision OS. Significant clinical findings included VA HM, 3+ mixed anterior chamber cells, and OS. Dense vitreous veils and aggregates were seen on B-scan OS. Acute- onset postoperative endophthalmitis was highly suspected, and the patient was immediately referred to ophthalmology. - The diagnosis was confirmed by Ann Arbor VA. A vitreous tap was performed and prophylactic intravitreal vancomycin (1mg/0.1mL) and ceftazidime (2.25mg/01mg) was administered. The vitreous sample returned negative results for gram stain, anaerobic, and susceptibility cultures. - Two months following endophthalmitis diagnosis, visual acuity is 20/150 OS. The anterior chamber is quiescent, but dense vitreous veils are still present. The next scheduled follow up with Ann Arbor VA is 08/17/2017 to determine whether a pars plana vitrectomy is indicated. - Once the condition has been fully resolved, baseline and periodic glaucoma work-ups will be administered at the BCVAMC.

VI. DISCUSSION - UGH was traditionally seen with first-generation anterior chamber and iris-fixated IOLs. With modern- day advances in IOL design and microsurgery, UGH is relatively uncommon in sulcus-fixated IOLs, and even more rare in posterior chamber IOLs. - Mechanical abrasion of iridociliary structures due to a malpositioned IOL can cause pigment dispersion, chronic inflammation, increased IOP, and hyphema. - Malpositioning of the IOL can occur during extraction or from head trauma. Zhang et al. (2014) suggested that zonular dehiscence and anterior capsule fibrosis around the haptics may also play a role. - Signs and symptoms are variable and depend upon the severity and duration of iridociliary trauma. One study indicated that <10% of cases present with the classical triad of uveitis, glaucoma, and hyphema, while >10% of cases have only TIDs without any of the classical signs. - Extensive iridocorneal damage and chronic inflammation can lead to pseudophakic bullous keratopathy, angle , vitreous hemorrhage, cystoid , and/or secondary glaucoma. - B-scan Ultrasonography is the gold standard for the diagnosis of UGH as it provides real-time visualization of the anterior chamber structures and IOL optics and haptics. - Treatment of UGH includes a combination of medical management and surgical intervention: o Control IOP with ocular hypotensive agents, reduce inflammation with topical steroids, and reduce ocular pain with topical NSAID and cycloplegic agent. o Timely referral to determine whether an IOL repositioning, explantation, or exchange is indicated to ultimately address the stimulus of inflammation. - Although the incidence of acute-onset postoperative endophthalmitis is rare ( <1%), close observation is required. Endophthalmitis is an ocular emergency and any delay in treatment may increase the risk of permanent vision loss. o Inflammation of the anterior or posterior chamber following invasion of microorganisms, bacteria being the most common, during or immediately after surgery. Onset of symptoms occur within 6 weeks, or as earlier as 72 hours after surgery. Patients may present with a sudden onset of pain, vision loss, anterior chamber reaction, hypopyon, and vitreous cells. Treatment includes vitreous tap with cultures and intravitreal antibiotics with or without vitrectomy.

VI. CONCLUSION - If not properly diagnosed and managed in a timely fashion, UGH can be sight-threatening. - Although surgical intervention may eliminate iris chafing and inflammation, close observation is still recommended to monitor for complications arising from surgery or iridociliary damage. o Extensive patient education of signs/symptoms of endophthalmitis. o Consider baseline and periodic visual field testing, ONH optical coherence tomography, and photography to monitor for the development of secondary glaucoma.