Patients with central serous chorioretinopathy not only have pachychoroidal disorders but also altered retinal metabolic function.

PURPOSE: The aim of our study was to compare metabolic (oxygen saturation; %) and anatomical (diameter; µm) retinal vessel parameters of patients with central serous chorioretinopathy (CSC) to those of controls. METHODS: In this prospective cross-sectional cohort study, 72 eyes of patients with CSC were compared with 21 eyes of healthy controls. Of the 72 patients, 52 had chronic, nonactive CSC (subgroup nCSC) and 20 had active CSC (subgroup aCSC), according to activity on fluorescein angiography. Retinal vessel oximetry (RO) was performed using the Oxymap T1 oximeter. Oxygen saturation in all major peripapillary retinal arterioles (A-SO2 ) and venules (V-SO2 ) was measured, and their difference (A-V SO2 ) was calculated. In addition, we evaluated the corresponding diameter in retinal arterioles (D-A) and venules (D-V). For statistical evaluation, ANOVA-based linear mixed-effects models were calculated (SPSS®; p < 0.05). RESULTS: Central serous chorioretinopathy (CSC) patients had significantly higher A-SO2 and V-SO2 compared to that of controls (p = 0.031 and p = 0.018 respectively). Especially, the subgroup of aCSC patients showed significantly higher A-SO2 and V-SO2 values (p = 0.027 and p = 0.034, respectively). In addition, superotemporal and superonasal quadrant location showed significant interactions with A-SO2 and V-SO2 (p ≤ 0.03). Diameter in retinal arterioles (D-A), an venules (D-V) and A-V SO2 findings showed no significant differences (p > 0.096). CONCLUSION: These data indicate that patients with CSC have altered metabolic function. The presence of disease activity showed the greatest influence on RO measurement, both compared to controls and to those with inactive chronic CSC disease.

Late morbidity during childhood and adolescence in previously premature neonates after patent ductus arteriosus closure.

The health status of previously premature neonates after closure of a patent ductus arteriosus (PDA) was analyzed in childhood and adolescence. Physician questionnaires were used to study 180 hospital survivors among 210 consecutive premature neonates who underwent PDA closure between 1985 and 2005. Complete follow-up data were obtained for 129 patients (72%). During a median follow-up period of 7 years (range, 2-22 years), three late deaths (2.3%) had occurred. Only 45% of the patients were considered healthy. Morbidity included developmental delay (41.1%), pulmonary illness (12.4%), neurologic impairment (14.7%), hearing impairment (3.9%), gastrointestinal disease (3.1%), and thoracic deformity (1.2%). None of the adverse variables during the neonatal period (intraventricular hemorrhage, bradycardia apnea syndrome, bronchopulmonary dysplasia, pulmonary bleeding, hyaline membrane disease, artificial respiration time [continuous positive airway pressure + intubation], or necrotizing enterocolitis) statistically predicted respective system morbidity at the follow-up evaluation. Hyaline membrane disease (odds ratio, 2.5; p = 0.026) and longer hospitalization time (odds ratio, 1.2 days per 10 hospitalization days; p = 0.032) in the newborn period were significant predictors of an unhealthy outcome at the last follow-up evaluation. Survival until childhood after closure of a hemodynamically significant PDA in premature neonates is satisfactory. However, physical and neurodevelopmental co-morbidity persist for half of the patients, perhaps as a sequela of prematurity unrelated to ductus closure.

The effect of ductal diameter on surgical and medical closure of patent ductus arteriosus in preterm neonates: size matters.

OBJECTIVE: We sought to analyze the effect of patent ductus arteriosus diameter on treatment success in premature neonates. METHODS: Among 537 consecutive neonates born between 1985 and 2005 with a diagnosed patent ductus arteriosus, 201 premature patients (<35 weeks' gestation) treated for a hemodynamically significant patent ductus arteriosus were retrospectively reviewed. Two groups were compared: group MED (n = 154; successful treatment with indomethacin) and group FAIL (n = 47; failure of medication to reduce the patent ductus arteriosus diameter to hemodynamic insignificance). RESULTS: After unsuccessful medical treatment, 33 patients required surgical patent ductus arteriosus closure, 12 died before further possible treatment, and 2 were discharged home without clinical symptoms but with an open patent ductus arteriosus. Mean patent ductus arteriosus diameter in the FAIL group (2.8 +/- 0.9 mm) was significantly larger than that in the MED group (2.4 +/- 0.6 mm, P < .01). Assisted respiration time (ventilation plus continuous positive airway pressure) before patent ductus arteriosus closure was longer in the FAIL group (20 days) than in the MED group (9 days, P < .001) but was similar after patent ductus arteriosus closure. By using an index of patent ductus arteriosus diameter squared/birth weight (in square millimeters per kilogram), a cutoff value of less than 9 mm2/kg correctly predicts medical patent ductus arteriosus closure in 87.5% of patients. Values of greater than 9 mm2/kg correctly predict medication failure in 41.5% of patients. CONCLUSIONS: In preterm babies requiring surgical patent ductus arteriosus closure, longer respiration times reflect a delay while attempting medical treatment, but respiration time is equally short between groups after shunt elimination. Medical treatment, although a valid first option, is likely to fail with larger patent ductus arteriosus diameters and lower birth weights. Unwarranted assisted respiration and corresponding hospital stay might be shortened by earlier surgical referral for patent ductus arteriosus closure in preterm babies with a patent ductus arteriosus index of greater than 9 mm2/kg.