Brown Syndrome from Local Anesthesia for Inferior Orbital Fat Decompression.

BACKGROUND Vertical diplopia that follows local anesthesia is usually due to inferior rectus muscle fibrosis. Here, we report a rare case of acquired Brown syndrome following local anesthesia. CASE REPORT A 36-year-old woman underwent right inferior orbital fat decompression under local anesthesia. On the first postoperative day, she developed vertical diplopia. She had left hypertropia, which increased on left gaze, with limitation of elevation of the right eye on attempted adduction. Forced duction test of the right eye revealed resistance on elevation in adduction. Magnetic resonance imaging showed signal alteration, thickening, and irregularity involving the right superior oblique tendon and trochlea region. The diagnosis of iatrogenic Brown syndrome was made. Then, a single dose of 10 mg triamcinolone injection was given near the intratrochlear region. On follow-up, complete resolution of diplopia on primary gaze occurred 12 weeks after the incident. CONCLUSIONS The reported case highlights that local anesthesia carries a risk of Brown syndrome. We believe bupivacaine-induced superior oblique hypertrophy is the underlying mechanism. The patient showed excellent outcome after medical management, with no surgical intervention required after 3 months of follow-up.

Pediatric refractive surgery in evolution.

With the advent of corneal refractive surgery using excimer laser technology, treatment for corneal and refractive disorders have advanced tremendously and become very precise and predictable. The use of these techniques in the treatment of corneal and refractive disorders in children, especially during the amblyogenic ages, would be invaluable. Numerous reports on refractive surgery in children have demonstrated that it can be performed safely and efficaciously in the pediatric population. However, controversy still exists whether it should be done in this population. We explore the available published data to address this controversy.

Molecular characterization of newborn glaucoma including a distinct aniridic phenotype.

PURPOSE: To characterize the underlying genetic defect in otherwise healthy Saudi newborns with buphthalmos, including those with iris abnormalities. METHODS: Prospective case series of affected Saudi Arabian probands who were referred for genetic counseling over a 4 year period. All had CYP1B1 sequencing. Selected patients with visible iris abnormalities had PAX6, FOXC1, and PITX2 sequencing. CYP1B1-negative patients had LTBP2 sequencing. RESULTS: All 67 probands had corneal enlargement with variable haze/scarring evident to caregivers at birth; 46 had a family history of infantile or early childhood glaucoma. All families were consanguineous except for 6, 2 of which were endogamous. Eight probands had mild ectropion uveae with partial aniridia; 2 probands had thick scarred corneas that precluded careful iris examination. Homozygous or compound heterozygous CYP1B1 mutations were identified in 91% (61/67), including all 8 probands with ectopion uveae and partial aniridia. The common Saudi mutation p.G61E occurred in most cases (38 homozygous, 8 compound heterozygous). Four novel mutations were identified (p.N252K, p.V460E, p.S485F, p.N519D). No mutations were identified in the other screened genes. CONCLUSIONS: Newborn glaucoma on the Arabian Peninsula is typically CYP1B1-related even in the setting of developmental iris abnormality. Mild iris ectropion with partial aniridia in a newborn with glaucoma suggests mutations in CYP1B1 rather than in other genes associated with anterior segment dysgenesis. On the Arabian Peninsula p.G61E mutations are the major cause of newborn glaucoma but novel CYP1B1 mutations continue to be documented. The fact that the 9% of cases that were CYP1B1-negative did not have mutations in LTBP2 suggests that there exists at least 1 additional locus for this condition.