Acta Ophthalmologica 2015 acuity (BCVA) was 0.30 0.30 logMAR at diagnosis and significantly increased to 0.19 0.26 logMAR at the end of follow-up (p = 0.011). Quadruple drug therapy was the most commonly used ATT regimen (13/30 subjects) (American Thoracic Society 2000); nine subjects had three drugs, seven subjects had two drugs, and one subject isoniazid alone. The mean duration of ATT was 7.8 1.3 months. Intraocular inflammation was quiescent at the end of ATT in all subjects. The rate of recurrence was 37.5%. Correlations between absence of recurrence of uveitis (SUN Working Group 2005) and therapeutic variables such as ATT regimen and ATT duration, local (i.e., periocular or intravitreal) and/or systemic administration of corticosteroids, or additional immunosuppressive therapy, were assessed using logistic regression. None of these parameters reached the threshold of statistical significance. The administration of local steroids in the form of periocular or intravitreal injections, however, was the practice with the highest correlation (p = 0.052). Our study documented an increasing incidence of TRU: 2–3% of patients referred to our uveitis clinics. These forms were mostly bilateral (67%). The posterior segment of the eye was the most affected, particularly in the form of retinal vasculitis. These data support the current practice of performing fluorescein angiography combined with indocyanine green angiography (ICG) in the routine assessment of any intermediate and posterior uveitis (Knecht et al. 2013). ICG is the key examination to rule out the hidden choroidal involvement (i.e. choroidal granulomas) as found in 20% of considered eyes. The use of ATT, even when treatment was delayed (mean, 8.3 months after the onset of symptoms), was effective in treating active inflammation and in improving visual acuity. A possible protective effect of local steroids against recurrence supports the applicability of this approach.
References American Thoracic Society (2000): Targeted tuberculin testing and treatment of latent tuberculosis infection. MMWR Recomm Rep 49: 1–51. Gineys R, Bodaghi B, Carcelain G et al. (2011): QuantiFERON-TB Gold Cut-off Value: implications for the Management of
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Tuberculosis-Related Ocular Inflammation. Am J Ophthalmol 152: 433–440. Kandel H, Adhikari P, Shrestha GS et al. (2012): Visual function in patients on ethambutol therapy for tuberculosis. J Ocul Pharmacol Ther 28: 174–178. Knecht PB, Papadia M & Herbort CP (2013): Secondary choriocapillaritis in infectious chorioretinitis. Acta Ophthalmol 91: 550–555. The Standardization of Uveitis Nomenclature (SUN) Working Group (2005): Standardization of Uveitis Nomenclature for reporting clinical data. Results of the First International Workshop. Am J Ophthalmol 140: 509–516.
Correspondence: Paolo Mora, MD Ophthalmology Unit Department of Biological, Biotechnological, and Translational Sciences University of Parma via Gramsci 14, 43126 Parma, Italy Tel: +39 0521 703138 Fax: +39 0521 992137 Email: [email protected]
Anatomy of nasolacrimal canal in congenital nasolacrimal duct obstruction – 18 cases retrospective study Chengyue Zhang,* Qian Wu,* Yanhui Cui and Gang Yu Department of Ophthalmology, Beijing Children’s Hospital, National Key Discipline of Pediatrics (Capital Medical University), Ministry of Education, Beijing, China *Qian Wu and Chengyue Zhang contributed equally to this work. doi: 10.1111/aos.12615
Editor, ongenital nasolacrimal duct obstruction is one of the most common ocular disorders in infants with an estimated prevalence ranging from 1.8% to 20% (MacEwen & Young 1991). It is usually congenital in origin resulting from a failure of canalization of the nasolacrimal duct. Asymmetrical enlargement of the nasolacrimal canal in the absence of
C
associated neoplasm is uncommon. It has sparsely been reported in the literature (Rheeman & Meyer 1998). In this study, CT results of unilateral congenital nasolacrimal duct obstruction were investigated after excluding the possibility of congenital nasolacrimal canal agenesis. The transverse diameters, anteroposterior diameters and areas of bilateral nasolacrimal canal at different levels were surveyed and compared to demonstrate whether there was relationship between nasolacrimal canal enlargement and congenital nasolacrimal duct obstruction. We retrospectively reviewed the CT results of 18 children with unilateral congenital nasolacrimal duct obstruction seen in the Department of Ophthalmology of Beijing Children’s Hospital from June 2011 to June 2012. This study followed the Declaration of Helsinki and was approved by the Ethics Committee of Beijing Children’s Hospital. We followed the low-dose CT protocol for children throughout the study. The traverse diameters, vertical diameters and areas of bony nasolacrimal duct at three levels were measured on the CT workstation. We selected initial segment, midpoint and the lowest point of nasolacrimal canal as three measurement levels (Fig. 1). The results showed that the transverse diameters of bony nasolacrimal duct increased significantly on the affected sides compared with the normal sides in unilateral congenital nasolacrimal duct obstruction (p = 0.000). The anteroposterior diameters of bony nasolacrimal duct were much larger on the affected sides than the normal sides (p = 0.000). And the areas of bony nasolacrimal duct were also larger on the affected sides than the normal sides (p = 0.000). In recent years, many researchers have sought to study the characteristics of nasolacrimal canal in normal children and congenital nasolacrimal duct obstruction by CT scans (Moscato et al. 2010; Weiss et al. 2012). However, few studies have addressed the issue of bony nasolacrimal duct enlargement. Our results showed that the transverse diameters, vertical diameters and areas of bony nasolacrimal duct on the affected side increased significantly compared with those on the normal side in unilateral congenital nasolacrimal duct obstruction. It is
Acta Ophthalmologica 2015
caused by sustained increase in hydrostatic pressure within the lacrimal duct.
References
Fig. 1. Terminal segment of nasolacrimal canal on axial CT. The transverse diameter, anteroposterior diameter and areas of bony nasolacrimal duct on the affected side (right eye) were much larger than the normal side (left eye).
currently believed that bony nasolacrimal duct enlargement is due to the fact that lacrimal duct obstruction leads to high pressure in the lacrimal duct on the affected side. The bony lacrimal duct is plastic in childhood, which results in significantly expanded bony nasolacrimal duct on the affected side compared with the normal side. As liquid is the major substance present in the lacrimal duct on the affected side, the pressure inside the nasolacrimal duct derives mainly from hydrostatic pressure. The equation is P = qgh, where P = hydrostatic pressure, q = density (g/cm3), g = gravitational acceleration and h = height. Liquid density generally changes little, and gravitational acceleration is constant. Thus, hydrostatic pressure is primarily dependent on liquid height. The height of bony nasolacrimal duct
was linearly correlated with children’s age. This means that the height of bony nasolacrimal duct increases with the age of children (Moscato et al. 2010). Pressure in the nasolacrimal duct also increases with age. Accordingly, hydrostatic pressure within the lacrimal duct plays a positive role in the selfhealing of congenital nasolacrimal duct obstruction (Moscato et al. 2010). Meanwhile, hydrostatic pressure within the lacrimal duct also presents an equal pressure on the wall of nasolacrimal canal, which results in the enlargement of bony nasolacrimal duct on the affected side. In conclusion, this study found that bony nasolacrimal duct enlarged significantly on the affected side compared with normal side in children with unilateral congenital nasolacrimal duct obstruction. This phenomenon is
MacEwen CJ & Young JD (1991): Epiphora during the first year of life. Eye (Lond) 5(Pt 5): 596–600. Moscato EE, Kelly JP & Weiss A (2010): Developmental anatomy of the nasolacrimal duct: Implications for congenital obstruction. Ophthalmology 117: 2430–34. Rheeman CH & Meyer DR (1998): Enlargement of the Nasolacrimal Canal in the absence of neoplasia. Ophthalmology 105: 1498–1503. Weiss AH, Baran F & Kelly J (2012): Congenital nasolacrimal duct obstruction. Arch Ophthalmol 130: 842–848.
Correspondence: Gang Yu Department of Ophthalmology Beijing Children’s Hospital National Key Discipline of Pediatrics (Capital Medical University) Ministry of Education 56th Nanlishilu Road Xicheng District Beijing 100045, China Tel: 86-10-59616398 Fax: 01059718700 Email: [email protected] Dr Zhang and Dr Wu carried out CT study and drafted this manuscript. Dr Cui participated in the design of the study and performed the statistical analysis. Dr Yu conceived of the study and participated in its design and co-ordination and helped to draft the manuscript. All authors read and approved the final manuscript.
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References American Thoracic Society (2000): Targeted tuberculin testing and treatment of latent tuberculosis infection. MMWR Recomm Rep 49: 1–51. Gineys R, Bodaghi B, Carcelain G et al. (2011): QuantiFERON-TB Gold Cut-off Value: implications for the Management of
e404
Tuberculosis-Related Ocular Inflammation. Am J Ophthalmol 152: 433–440. Kandel H, Adhikari P, Shrestha GS et al. (2012): Visual function in patients on ethambutol therapy for tuberculosis. J Ocul Pharmacol Ther 28: 174–178. Knecht PB, Papadia M & Herbort CP (2013): Secondary choriocapillaritis in infectious chorioretinitis. Acta Ophthalmol 91: 550–555. The Standardization of Uveitis Nomenclature (SUN) Working Group (2005): Standardization of Uveitis Nomenclature for reporting clinical data. Results of the First International Workshop. Am J Ophthalmol 140: 509–516.
Correspondence: Paolo Mora, MD Ophthalmology Unit Department of Biological, Biotechnological, and Translational Sciences University of Parma via Gramsci 14, 43126 Parma, Italy Tel: +39 0521 703138 Fax: +39 0521 992137 Email: [email protected]
Anatomy of nasolacrimal canal in congenital nasolacrimal duct obstruction – 18 cases retrospective study Chengyue Zhang,* Qian Wu,* Yanhui Cui and Gang Yu Department of Ophthalmology, Beijing Children’s Hospital, National Key Discipline of Pediatrics (Capital Medical University), Ministry of Education, Beijing, China *Qian Wu and Chengyue Zhang contributed equally to this work. doi: 10.1111/aos.12615
Editor, ongenital nasolacrimal duct obstruction is one of the most common ocular disorders in infants with an estimated prevalence ranging from 1.8% to 20% (MacEwen & Young 1991). It is usually congenital in origin resulting from a failure of canalization of the nasolacrimal duct. Asymmetrical enlargement of the nasolacrimal canal in the absence of
C
associated neoplasm is uncommon. It has sparsely been reported in the literature (Rheeman & Meyer 1998). In this study, CT results of unilateral congenital nasolacrimal duct obstruction were investigated after excluding the possibility of congenital nasolacrimal canal agenesis. The transverse diameters, anteroposterior diameters and areas of bilateral nasolacrimal canal at different levels were surveyed and compared to demonstrate whether there was relationship between nasolacrimal canal enlargement and congenital nasolacrimal duct obstruction. We retrospectively reviewed the CT results of 18 children with unilateral congenital nasolacrimal duct obstruction seen in the Department of Ophthalmology of Beijing Children’s Hospital from June 2011 to June 2012. This study followed the Declaration of Helsinki and was approved by the Ethics Committee of Beijing Children’s Hospital. We followed the low-dose CT protocol for children throughout the study. The traverse diameters, vertical diameters and areas of bony nasolacrimal duct at three levels were measured on the CT workstation. We selected initial segment, midpoint and the lowest point of nasolacrimal canal as three measurement levels (Fig. 1). The results showed that the transverse diameters of bony nasolacrimal duct increased significantly on the affected sides compared with the normal sides in unilateral congenital nasolacrimal duct obstruction (p = 0.000). The anteroposterior diameters of bony nasolacrimal duct were much larger on the affected sides than the normal sides (p = 0.000). And the areas of bony nasolacrimal duct were also larger on the affected sides than the normal sides (p = 0.000). In recent years, many researchers have sought to study the characteristics of nasolacrimal canal in normal children and congenital nasolacrimal duct obstruction by CT scans (Moscato et al. 2010; Weiss et al. 2012). However, few studies have addressed the issue of bony nasolacrimal duct enlargement. Our results showed that the transverse diameters, vertical diameters and areas of bony nasolacrimal duct on the affected side increased significantly compared with those on the normal side in unilateral congenital nasolacrimal duct obstruction. It is
Acta Ophthalmologica 2015
caused by sustained increase in hydrostatic pressure within the lacrimal duct.
References
Fig. 1. Terminal segment of nasolacrimal canal on axial CT. The transverse diameter, anteroposterior diameter and areas of bony nasolacrimal duct on the affected side (right eye) were much larger than the normal side (left eye).
currently believed that bony nasolacrimal duct enlargement is due to the fact that lacrimal duct obstruction leads to high pressure in the lacrimal duct on the affected side. The bony lacrimal duct is plastic in childhood, which results in significantly expanded bony nasolacrimal duct on the affected side compared with the normal side. As liquid is the major substance present in the lacrimal duct on the affected side, the pressure inside the nasolacrimal duct derives mainly from hydrostatic pressure. The equation is P = qgh, where P = hydrostatic pressure, q = density (g/cm3), g = gravitational acceleration and h = height. Liquid density generally changes little, and gravitational acceleration is constant. Thus, hydrostatic pressure is primarily dependent on liquid height. The height of bony nasolacrimal duct
was linearly correlated with children’s age. This means that the height of bony nasolacrimal duct increases with the age of children (Moscato et al. 2010). Pressure in the nasolacrimal duct also increases with age. Accordingly, hydrostatic pressure within the lacrimal duct plays a positive role in the selfhealing of congenital nasolacrimal duct obstruction (Moscato et al. 2010). Meanwhile, hydrostatic pressure within the lacrimal duct also presents an equal pressure on the wall of nasolacrimal canal, which results in the enlargement of bony nasolacrimal duct on the affected side. In conclusion, this study found that bony nasolacrimal duct enlarged significantly on the affected side compared with normal side in children with unilateral congenital nasolacrimal duct obstruction. This phenomenon is
MacEwen CJ & Young JD (1991): Epiphora during the first year of life. Eye (Lond) 5(Pt 5): 596–600. Moscato EE, Kelly JP & Weiss A (2010): Developmental anatomy of the nasolacrimal duct: Implications for congenital obstruction. Ophthalmology 117: 2430–34. Rheeman CH & Meyer DR (1998): Enlargement of the Nasolacrimal Canal in the absence of neoplasia. Ophthalmology 105: 1498–1503. Weiss AH, Baran F & Kelly J (2012): Congenital nasolacrimal duct obstruction. Arch Ophthalmol 130: 842–848.
Correspondence: Gang Yu Department of Ophthalmology Beijing Children’s Hospital National Key Discipline of Pediatrics (Capital Medical University) Ministry of Education 56th Nanlishilu Road Xicheng District Beijing 100045, China Tel: 86-10-59616398 Fax: 01059718700 Email: [email protected] Dr Zhang and Dr Wu carried out CT study and drafted this manuscript. Dr Cui participated in the design of the study and performed the statistical analysis. Dr Yu conceived of the study and participated in its design and co-ordination and helped to draft the manuscript. All authors read and approved the final manuscript.
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