IMPORTANCE Elevated intraocular pressure (IOP) and decreased ocular perfusion pressure (OPP) are risk factors for glaucoma development and progression. Unrecognized significant IOP elevation or OPP reduction during hemodialysis (HD) could lead to glaucomatous optic nerve damage and subsequent visual loss. OBJECTIVE To evaluate changes in IOP and OPP during HD. DESIGN, SETTING, AND PARTICIPANTS A cross-sectional observational study was conducted in patients undergoing HD at an ambulatory care clinic at the University of Illinois at Chicago. EXPOSURES Forty-nine patients (97 eyes) undergoing HD were enrolled. Exclusion criteria included preexisting corneal abnormalities, history of corneal surgery, allergy to topical anesthetic agents, and current eye infection. Nine patients had previous diagnoses of open-angle glaucoma (OAG) or suspected glaucoma. At 3 time points, IOP was measured using a pneumatonometer and blood pressure was recorded. Measurements were made with the patient in a seated position approximately 15 minutes before starting HD (T1), approximately 2 hours after starting HD (T2), and approximately 15 minutes after ending HD (T3). Mean arterial pressure (MAP) and OPP (systolic, diastolic, and mean OPP) were calculated. MAIN OUTCOMES AND MEASURES Intraocular pressure and OPP. RESULTS From T1 to T3, IOP significantly increased by 3.1 mm Hg (both eyes, P < .001), MAP significantly decreased by 5.8 mm Hg (P = .05), and all OPP measures significantly decreased from baseline (all P Յ .02). Using previously reported thresholds of increased glaucoma development and progression risk, 53% of the right eyes (26 of 49) and 46% of the left eyes (22 of 48) had a systolic OPP of 101 mm Hg or less, 71% of the right eyes (35 of 49) and 73% of the left eyes (35 of 48) had a diastolic OPP of 55 mm Hg or less, and 63% of the right eyes (31 of 49) and 65% of the left eyes (31 of 48) had a mean OPP of 42 mm Hg or less. CONCLUSIONS AND RELEVANCE Significantly increased IOP and decreased OPP occur during HD, bringing both to levels that increase the risk of glaucoma development and progression. Clinicians should consider HD history in patients who have glaucoma progression, even when IOP has been well controlled. Such patients may benefit from IOP and blood pressure monitoring during HD sessions to minimize OPP changes resulting from IOP spikes and/or suboptimal blood pressure.

This was an observational study of a cohort of 126 veterans with mild traumatic brain injury caused by an explosion during deployment in Operation Iraqi Freedom or Operation Enduring Freedom (OIF/OEF); 74 of the 126 veterans had comorbidities including frequent, severe headaches and residual deficits on neurological examination, neuropsychological testing, or both. Of these veterans, 71 had posttraumatic stress disorder and only 5 had restful sleep. We examined whether treatment with sleep hygiene counseling and oral prazosin would improve sleep, headaches, and cognitive performance. Nine weeks after providing sleep counseling and initiating an increasing dosage schedule of prazosin at bedtime, 65 veterans reported restful sleep. Peak headache pain (0-10 scale) decreased from 7.28 +/-0.27 to 4.08 +/-0.19 (values presented as mean +/-standard deviation). The number of headaches per month decreased from 12.40 +/-0.94 to 4.77 +/-0.34. Montreal Cognitive Assessment scores improved from 24.50 +/-0.49 to 28.60 +/-0.59. We found these gains maintained 6 months later. This pilot study suggests that addressing sleep is a good first step in treating posttraumatic headaches in OIF/OEF veterans.

SummaryDeferoxamine is a commonly used chelating agent for secondary hemochromatosis. We report a rare retinal manifestation of deferoxamine toxicity in a 68-year-old man and provide supporting multimodal imaging and electrophysiology. The patient had iron overload related to transfusion-dependent myelodysplastic syndrome and developed a pseudovitelliform macular lesion related to deferoxamine toxicity. We also describe for the first time the worsening of this maculopathy on deferasirox, an alternative chelating agent. Macular pseudovitelliform lesion is a unique manifestation of deferoxamine toxicity that can be mistaken for pattern dystrophy. It is important to recognize this manifestation, because discontinuation of the offending agent may halt or reverse the toxicity. Case ReportA 68-year-old man presented to Atlantis Eyecare for evaluation of blurred vision in both eyes. He endorsed dark adaptation difficulties for 6 months. A year prior to presentation, he was noted by his general ophthalmologist to have a normal fundus examination. His past medical history was notable for myelodysplastic syndrome, for which he received frequent blood transfusions. He had been on deferoxamine for 5 years, presently at 16 g per week, for transfusion-related hemochromatosis. On review of systems, he reported adult-onset hearing loss. He had no family history of retinal degeneration or other pertinent history.On examination, uncorrected Snellen visual acuity was 20/25-2 in the right eye and 20/30-2 in the left eye. Ishihara plates were 4/15 in the right eye and 1/15 in the left eye. There was no afferent pupillary defect. He had bilateral posterior chamber intraocular lenses. Fundus examination revealed healthy appearing optic nerves, but there was diffuse pigment mottling in both maculae, with pseudovitelliform lesions centrally ( Figure 1A). Retinal vessels and periphery were unremarkable.Fundus autofluorescence (FAF) revealed central hypoautofluorescence, with surrounding punctuate increased and decreased autofluorescence in the macula ( Figure 1B). Wide-field FAF did not reveal any abnormalities outside of the maculae ( Figure 1C). Fluorescein angiography (FA) showed blocked fluorescence centrally, with surrounding punctate staining and transmission hyperfluorescence corresponding to the areas of pigment mottling ( Figure 1D). Indocyanine green (ICG) angiography showed increased choroidal vascularity in both maculae ( Figure 1E). Optical coherence tomography (OCT) of the macula revealed vitreomacular adhesion with central subretinal deposits in both eyes (Figure 2A).Kinetic perimetry (Goldmann) revealed superior constriction in both eyes, worse on the right (Figure 3). Electroretinography (ERG) demonstrated a mild-tomoderate reduction in rod function, with relatively preserved cone function of the right eye and normal rod and cone function of the left eye ( Figure 4A and 4B). The electro-oculogram (EOG) was markedly abnormal, with an Arden ratio of 1.3 in each eye ( Figure 4C).Given morphologic and functional evidence of...