Evaluation and treatment of failed nasolacrimal duct probing in Down syndrome Francine Baran, MD,a,b John P. Kelly, PhD,a,b Laura S. Finn, MD,c Scott Manning, MD,d Erin Herlihy, MD,a,b and Avery H. Weiss, MDa,b PURPOSE

To elucidate the mechanisms underlying failed nasolacrimal duct (NLD) probing in children with Down syndrome (DS) utilizing computed tomography (CT) scans and histopathology of nasal mucosa.

METHODS

The medical records of children with DS and NLD obstruction confirmed by dye disappearance testing who failed NLD surgery were retrospectively reviewed. Dimensions of the bony NLD and presence of postductal mucosal obstruction were obtained from CT scans. Histopathology of the nasal mucosa was performed in a subset of patients. Subsequent treatment was topical or intranasal corticosteroids or submucosal corticosteroids alone or combined with surgical reduction of the inferior turbinate.

RESULTS

A total of 9 subjects (age range, 8-10 years) and 43 age-matched controls were included. Both groups demonstrated a logarithmic increase in NLD and maxilla dimensions with increasing age; however, the transverse diameter of the NLD was consistently 1-2 mm smaller in children with DS #5 years age (n 5 4) than in age-matched controls. The transverse diameter in DS children overlapped that of controls after 5 years age. Histopathology revealed abnormal lymphoplasmacytic inflammation of the mucosa in 4 of 5 biopsies of DS patients, consistent with chronic infection, allergic disease, or immune dysregulation. The postductal obstruction was successfully treated with topical or intranasal corticosteroids or by surgical reduction of the inferior turbinate submucosa with corticosteroid injection. Before 5 years of age, NLD obstruction in children with DS was associated with reduced dimensions of the NLD and hypertrophic nasal mucosa. In DS children older than 5 years of age, the dimensions of the NLD are normal and postductal obstruction due to hypertrophic nasal mucosa should be considered. ( J AAPOS 2014;18:226-231)

CONCLUSIONS

N

asolacrimal duct obstruction (NLDO) is common in children with Down syndrome (DS), with a reported prevalence of 22%.1 Standard treatment of persistent NLDO is lacrimal probing with or without stent; however, children with DS have a lower cure rate than those without DS. The higher rate of NLDO in DS is in part related to the unique facial morphology2-5 and abnormal persistence of a membrane or bony obstruction along the distal portion of the nasolacrimal duct (NLD).6 Previous investigators reported

Author affiliations: aRoger Johnson Clinical Vision Laboratory, Division of Ophthalmology, Seattle Children’s Hospital, Seattle, Washington; bDepartment of Ophthalmology, University of Washington Medical Center, Seattle; cDepartment of Pathology, University of Washington Medical Center and Department of Laboratories, Seattle Children’s Hospital, Seattle; dDivision of Otolaryngology, Seattle Children’s Hospital, Seattle Supported by an unrestricted grant from grant from the Peter LeHaye, Barbara Anderson, and William O. Rogers Endowment Funds. Submitted September 20, 2013. Revision accepted December 29, 2013. Correspondence: Avery H. Weiss, MD, Division of Ophthalmology, OA.9.220, Seattle Children’s Hospital, 4800 Sand Point Way NE, Seattle, Washington 98105 (email: avery. [email protected]). Copyright Ó 2014 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2013.12.018

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an improved success rate with balloon catheter dilation or probing with stent placement compared to lacrimal probing alone.7,8 Coats and colleagues7 reported several mechanisms underlying the obstruction, including proximal agenesis of the punctum, a stricture, or atresia, along the canaliculus, generalized narrowing of the NLD, or an anterior displacement of the inferior turbinate. Lueder8 suggested that the lacrimal pump was defective. The purpose of this study was to further elucidate the mechanisms underlying failed NLD probing in children with DS. Patients with persistent epiphora following NLD probing with stent placement were studied by means of combined computed tomography (CT) imaging of the NLD and histopathological studies of the nasal mucosa.

Methods The medical records of patients seen at the Seattle Children’s Hospital Ophthalmology Clinic between February 2007 and June 2011 were retrospectively reviewed to identify children with DS who were treated surgically for NLDO. The study was approved by the hospital’s institutional review board. The diagnosis of NLD obstruction was based on a history of epiphora with or without recurrent infections and an abnormally prolonged

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Volume 18 Number 3 / June 2014 dye disappearance test (DDT). The DDT consisted of the instillation of one drop of a 5% fluorescein solution into the conjunctival fornix followed by unmasked assessment of retained fluorescence on illumination with short wavelength (blue) light source after 5 minutes. We selectively studied the children who had persistent epiphora after 1-3 NLD probings with or without placement of a stent. Each of these patients had undergone CT imaging, biopsy of the nasal mucosa, or both procedures to investigate the persistent epiphora. Initial probing consisted of dilation of the punctum followed by serial insertion of Bowman probes of increasing diameter (double 0-3, depending on age). Successful probing was confirmed by direct visualization of the distal end of the probe or indirectly by instrumental palpation. All probings were performed in the outpatient clinic for children \14 months of age. All punctoplasty, nasolacrimal duct stent placement, or dacryocystorhinostomy (DCR) procedures were performed under general anesthesia using standard techniques. When available, CT scans were obtained for presurgical evaluation in all patients who failed the standard NLD procedures and in patients being considered for a DCR. Imaging of the head and orbits was obtained with a CBTB-016A two-dimensional scanner (Toshiba Corp, Tokyo, Japan), with continuous sections of 0.625 mm thickness (5 of 7 patients) or 1.25 mm thickness (2 patients). Transaxial images of the head and maxillofacial skull were helically acquired using 2:1 pitch (256  256 matrix covering a 10 cm area, yielding a pixel resolution of 391 mm). Dimensions and volumes of the NLD were obtained from the native DICOM file format using a Centricity PACS 3.1.1.2 RA1000 Workstation (GE Healthcare, Barrington, IL). The transverse diameter of the bony NLD was measured at the proximal end to avoid overestimation of the diameter due to head rotation in the sagittal plane. Transverse diameter and height of the bony portion of the NLD and height of the maxilla in 43 age-matched controls were obtained from the data set reported by Moscato and colleagues.9 Growth curves and correlation coefficients were calculated by the standard logarithmic fitting in Microsoft Excel (Microsoft, Redmond, WA). Three-dimensional reconstruction of the bony portion of the NLD was achieved by methods previously described6 using NIH Image J software (version 1.43 http://rsb. info.nih.gov/ij). For submucosal corticosteroid injection a mixture of 1 mL triamcinolone acetonide (40 mg/mL) and 4 mL of 1% lidocaine with epinephrine were used. At NLD surgery, 0.75 mL of solution was injected through a 27-gauge needle into the mucosa of the inferior turbinate bilaterally (total volume, 1.5 mL). Injections were performed in 2 patients who failed 3 previous NLD procedures and in 2 patients undergoing surgical inferior turbinate reduction. Turbinate reduction was performed at the discretion of the surgeon in select patients. Following infracture of the inferior turbinate, the inflamed mucosa beneath the turbinate was removed with a 2.9 mm sinus microdebrider blade along its entire length, back to the choanal opening. The specimen was submitted for standard histopathology. Biopsy specimens were taken from nasal mucosa of the inferior meatus. Specimens were prepared for histopathology using standard sectioning and staining.

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Results Of 24 children with DS who underwent treatment for NLDO, 9 (37%) who had persistent epiphora after 1-3 NLD probings with or without placement of a stent were included. Of these, 7 had undergone CT imaging; 6, biopsy of the nasal mucosa; and 4, both procedures. Table 1 summarizes the clinical findings and sequential surgical procedures of the 9 patients, listed in the chronological order in which they were evaluated. Each patient had the onset of bilateral epiphora from infancy, with delayed DDT prior to NLD surgery. At the initial probing, no resistance was encountered along the NLD in 8 cases; patient 9 was felt to have a membranous obstruction of the distal portion of the NLD. After NLD probing with or without stent placement or in-fracture of the inferior turbinate, each patient continued to have epiphora and a persistently delayed dye disappearance test. Patient 1, who underwent NLD probing twice, with and without placement of a lacrimal stent, as well as left-sided external DCR at 6 years of age, was the most extreme example of treatment failure. Preoperative CT scans revealed postductal obstruction due to hypertrophic nasal mucosa. The DDT was delayed bilaterally, with the left side affected more than the right. At surgery the right NLD was patent, the distal portion of the left NLD and surgical fistula connecting the lacrimal sac with the middle meatus were patent, accommodating a size 3 Bowman probe. The clinical finding of a patent NLD in 8 of the patients combined with the CT findings of abnormal thickening of the nasal mucosa in 7 patients indicated the postductal nasal mucosa as the site of obstruction. All patients treated with topical intranasal or submucosal corticosteroid, with or without turbinate reduction, reported decreased epiphora although the DDT showed mild residual delay. CT Findings Figure 1A is a representative coronal view of the distal NLD and inferior meatus in a 14-month-old child with DS (patient 2) who failed NLD probing with stent. The image, aligned on the entry of the distal NLD into the inferior meatus, shows the patency of the distal NLD and complete opacification of the inferior meatus with nasal mucosa (Figure 1A). By contrast, an 11-month control has more air spaces with less prominence of nasal mucosa in the inferior meatus (Figure 1B). Corresponding three-dimensional reconstructions of the NLD highlight the absence of a bony obstruction but a much shorter NLD in the child with DS (e-Supplement 1C-D, available at jaapos.org). The transverse diameters of the bony portion of the NLD measured at the superior (proximal) end of the duct are plotted in Figure 2A. The right and left NLD are shown for each DS subject. Both the control and DS groups demonstrate a logarithmic increase in diameter with increasing age (DS, r 5 0.85; P \ 0.001; controls, r 5 0.60; P \ 0.0001). Of note, the transverse diameter

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Table 1. Clinical history, procedures, and diagnostic testing Procedure Age at presentation, Case years Sex Symptoms 1 2 3 4 5 6 7 8 9

0.8 1.2 1.7 2.1 4.4 5.3 5.7 6.9 10.1

M F M F F M M M M

E,I E E,I E E E E,I E E

1

2

RE

LE

P P,Fx P,Pu P,Fx P,Fx,MS P,MS P,MS P,BS P,MS

P P,Fx,BS P,Pu,MS P,Fx,BS P,Fx,BS P,BS P,BS P,BS

3

RE

LE

P,BS

P,BS

P,BS

P,BS

ITR, SS ITR, SS ITR, SS ITR, SS P

BL

RE

4 LE

RE

DCR P,ITR,SS P,BS P,BS ITR

5 LE

RE BL ITR,SS

LE CT scan Biopsy Y Y Y Y Y Y N N Y

Y N Y N Y Y Y Y N

BL, blepharoplasty; BS, bicanalicular stent; CT, computed tomography; DCR, dacryocystorhinostomy; E, epiphora; Fx, fracture inferior turbinate; I, infection; ITR, inferior turbinate reduction; LE, left eye; MS, monocanalicular stent; P, probing; Pu, punctoplasty; RE, right eye; SS, submucosal steroids.

bony NLD. The smaller diameter and height of the NLD translates into a much smaller volume in young children with DS. For example in patient 2, the estimated NLD volume was 1.76 mm3 versus 9.4-107.5 mm3 in age-matched controls. Figure 2C shows the height of the maxillary sinus with increasing age in children with DS and control subjects. Control children demonstrate a logarithmic growth in maxillary sinus height with increasing age (r 5 0.91). Logarithmic growth in the maxillary sinus height with increasing age was noted in both the DS group (r 5 0.57, P 5 0.03) and controls (r 5 0.91, P \ 0.0001). However, the slope of this relationship is reduced by 50% in children with DS.

FIG 1. Computed tomography scans (CT) and corresponding threedimensional reconstructions. A, Coronal CT of a 14-month-old child with Down syndrome (DS) showing the distal portion of the nasolacrimal duct (NLD) entering into the inferior meatus (arrow). B, Coronal CT of an 11-month-old control showing more air spaces and less prominence of nasal mucosa in the inferior meatus.

of the NLD in children with DS is consistently smaller than that of age-matched controls between 1 and 5 years of age. After 5 years, the transverse diameter of the NLD in children with DS overlaps that of age-matched controls. Figure 2B shows that the height of the bony portion of the NLD in children with DS was well below agematched controls at\6 years of age. A logarithmic increase in transverse diameter with age was noted in both the DS group (r 5 0.90, P \ 0.0001) and the control group (r 5 0.54, P \ 0.0001). The paucity of data at the upper age range limits the prediction of the final height of the

Histopathology Histopathological examination of nasal mucosa in patients 5 and 6 revealed mild to markedly inflamed hypervascular respiratory mucosa that contained a predominantly lymphoplasmacytic infiltrate with variable numbers of accompanying eosinophils (e-Supplement 2, available at jaapos. org). In 4 of 5 biopsied patients with DS organized lymphoid follicles were not observed (e-Supplement 3B, available at jaapos.org). In some specimens, inflammatory cells invaded the glandular and surface epithelium, which was occasionally accompanied by reactive changes characterized by simplification with loss of pseudostratification, cilia and goblet cells (e-Supplement 3A). Subepithelial fibrosis was moderate in 2 cases (patients 6 and 7; e-Supplement 3). The presence of so-called mucosal-associated lymphoid tissue (MALT) may be a normal finding or an abnormal finding secondary to an underlying chronic infection, allergy or immune dysregulation. Given the lack of organization, epithelial invasion and prominence of plasma cells, the histopathologic findings in the patients reported here are abnormal. Histopathological findings, associated disorders of the upper respiratory tract, and response to corticosteroid treatment are summarized in Table 2.

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Discussion

FIG 2. A, Transverse diameter of the proximal portion of nasolacrimal duct across age. Diameter (mm), controls 5 0.49 * Loge(age) 1 3.14; diameter (in mm), DS 5 0.95 * Loge(age) 1 1.68. B, Height of the bony nasolacrimal duct across age. Height (mm), controls 5 0.91 * Loge(age) 1 5.57; height (mm), DS 5 3.26 * Loge(age) 1 1.35. C, Height of the maxillary sinus across age. Height (mm), controls 5 8.87 * Loge(age) 1 11.95; height (in mm), DS 5 4.47 * Loge(age) 1 7.68.

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This study demonstrates that reduced dimensions of the NLD along with postductal mucosal obstruction underlies persistent epiphora following NLD probing with stent placement or external DCR in children with DS younger than 5 years of age. The effects of the reduced NLD dimensions are greatest in infancy, when there is logarithmic growth of the NLD.9 However, the early exponential increase in children with DS was approximately 50% of that expected for age-matched controls. After 6 months of age, the differences between DS children and controls decreased and leveled off at 5 years of age. The effects of these dimensional differences is amplified with respect to volume of the NLD, which was 1.76 mm3 in patient 2 versus 9.4-107.5 mm3 in age-matched controls. These volume difference translate into substantial differences in hydrostatic pressure that is known to be a principal determinant of lacrimal flow.10,11 We also demonstrated that postnatal growth of the NLD in children with DS paralleled the growth of the maxilla but was 50% of controls across age. After 5 years of age postductal obstruction was the predominant factor predisposing to NLD obstruction. Although epiphora in DS typically appeared in infancy, it was often addressed at an older age because the incidence of superimposed infections was low, and associated systemic comorbidities were likely a higher priority. The histopathologic finding of abnormal lymphoplasmacytic inflammation of the nasal mucosa in 4 of 5 biopsied patients is consistent with chronic infection, allergic disease, or immune dysregulation. The lack of cellular organization, epithelial invasion, and prominence of plasma cells exceeded MALT seen in normal individuals. MALT has been identified previously in the lamina propria beneath the columnar epithelium of the NLD.12 Paulsen and colleagues12 have proposed that MALT represents an acquired response to infectious or environmental antigens that is present in up to 41% to 44% of asymptomatic normal adults. To our knowledge, the present study is the first to report the presence of MALT in infants and children with NLD obstruction. In support of an infectious etiology, each of the 9 patients had variable presence of eustachian tube dysfunction, tonsillar hypertrophy, recurrent otitis media, sinusitis, and superimposed dacryocystitis. We also confirmed the observation of Paulsen13 that the lymphoplasmacytic infiltrate can be replaced by fibrovascular connective tissue in patients with chronic NLD (cases 7 and 8). Damage of the pseudostratified epithelium with hyalinized thickening of the basement membrane was observed in pathology sections. Evidence of allergic disease and immune dysregulation were the variable presence of allergic rhinitis, reactive airway disease, or histopathologic evidence of eosinophils. Supporting evidence for immune dysregulation in DS includes reductions in natural killer

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Table 2. Histopathology, associated upper respiratory disease and response to corticosteroid treatment Case 1 2 3 4 5 6 7 8 9

Pathology

Associated disease

Corticosteroid treatment

Response

LPI No biopsy Insufficient mucosa No biopsy LPI LPI LPI, basement membrane thickening, eosinophils LPI; basement membrane thickening No biopsy

ETD, TH ETD Allergic rhinitis; OSA, TH, RAD ETD, OSA, TH ETD, otitis media, OSA, TH ETD, OSA, TH OSA, TH ETD, RAD, TH ETD, TH

Submucosal None Submucosal Intranasal Submucosal and Intranasal Submucosal None Topical Topical

Epiphora decreased Epiphora persists Epiphora decreased Epiphora decreased Epiphora decreased Epiphora decreased Epiphora persists Epiphora decreased Epiphora decreased

ETD, eustachian tube dysfunction; LPI, lymphoplasmacytic infiltrate; OSA, obstructive sleep apnea; RAD, reactive airway disease; TH, tonsillar hypertrophy.

cells, CD41 helper T cells and cytotoxic CD81 T cells, and impairments of innate immunity.14,15 A defect of the muscular lacrimal pump has been proposed to underlie NLDO in DS.8 Tear drainage is an active process initiated by the positive pressure with each eyelid blink and terminated by the negative pressure of16-19 eyelid opening. In DS the combination of generalized hypotonia with floppy eyelids and altered midface anatomy are likely to decrease the efficiency of the active lacrimal pump and contribute to symptomatic epiphora. Recent anatomic studies of the NLD have identified a second mechanism regulating tear flow.13,20 The central lumen of the NLD is surrounded by a vascular network, the cavernous body, which occupies two-thirds of the crosssectional area of the bony NLD. Expansion and contraction of the cavernous body may facilitate the alternate widening and narrowing of the NLD lumen. As a result of this dynamic capacitance, the cavernous body can expand or contract leading to closure or opening of the NLD lumen. Given that the cavernous body of the NLD is contiguous with the cavernous body of the inferior turbinate, engorgement of the vascular cavernous body would increase its volume relative to the NLD lumen and may potentially limit the efficiency of the cavernous body pump in DS. Coats and colleagues7 have reported that the obstruction in DS is most commonly due to stenosis or atresia of the canaliculi based on difficulties encountered in advancing the lacrimal probe into the lacrimal sac at the time of surgery. We propose an alternative explanation for their findings. The canaliculi and the common canaliculus are vulnerable to several mechanical constraints. One is the fixed, vertical orientation of the epicanthal folds relative to the horizontal axes of the canaliculi, which are embedded in floppy eyelids. Another is the transition from soft tissues to osseous tissues proximal to the common canaliculus. A third constraint arises from the recessed nasal bridge along with maxillary hypoplasia associated with DS that may impose additional restrictions in the region of the bony lacrimal fossa. Thus the common canaliculus represents an especially vulnerable site because it colocalizes with the intersection of multiple, orthogonally directed tensions. Our study demonstrates that CT imaging provides evidence of postductal obstruction due to nasal mucosal

thickening in children with DS who fail lacrimal probing with or without stent placement. Furthermore, the mucosal thickening is due to a combination of a lymphoplasmacytic infiltrate and vascular engorgement. Taken together, these findings have prompted us to change our management of children with DS who fail NLD probing. Previously, these patients were considered candidates for DCR. Now we recommend a trial of intranasal or lowpotency topical ocular corticosteroids if nasal endoscopy confirms engorgement of the nasal mucosa. Persistence of epiphora and superimposed infections prompts consideration of facial CT imaging with fine cuts and submucosal injection of corticosteroids, with or without surgical reduction of the inferior turbinate mucosa. The final step of our treatment algorithm involves the diagnostic use of a high-resolution facial CT scan. Although the dosimetry for these CT scans is low, there is a potential higher risk for malignancy, especially in individuals with DS.21-23 The CT dose index (CTDI) is the main metric and reflects the radiation exposure of a single slice plus the scatter from surrounding slices. The CTDI (\20 mGy) in this study was well below the American College of Radiology CT Accreditation CTDI reference levelof75 mGy. Therefore, we thoroughly discuss the benefits and drawbacks of CT imaging and surgical implications with the patient’s caretakers. We believe that the ability to readily identify and successfully treat the cause of the obstruction outweighs the costs and potential risks of additional NLD surgeries. References 1. Berk AT, Saatci AO, Erc¸al MD, Tunc¸ M, Ergin M. Ocular findings in 55 patients with Down’s syndrome. Ophthalmic Genet 1996;17: 15-19. 2. Caputo AR, Wagner RS, Reynolds DR, Guo SQ, Goel AK. Down syndrome: clinical review of ocular features. Clin Pediatr (Phila) 1989;28:355-8. 3. Catalano RA. Down syndrome. Surv Ophthalmol 1990;34:385-98. 4. da Cunha RP, Moreira JB. Ocular findings in Down’s syndrome. Am J Ophthalmol 1996;122:236-44. 5. Shapiro MB, France TD. The ocular features of Down’s syndrome. Am J Ophthalmol 1985;99:659-63. 6. Weiss AH, Baran F, Kelly J. Congenital nasolacrimal duct obstruction: delineation of anatomic abnormalities with 3-dimensional reconstruction. Arch Ophthalmol 2012;130:842-8.

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Volume 18 Number 3 / June 2014 7. Coats DK, McCreery KM, Plager DA, Bohra L, Kim DS, Paysse EA. Nasolacrimal outflow drainage anomalies in Down’s syndrome. Ophthalmology 2003;110:1437-41. 8. Lueder GT. Treatment of nasolacrimal duct obstruction in children with trisomy 21. J AAPOS 2000;4:230-32. 9. Moscato EE, Kelly JP, Weiss A. Developmental anatomy of the nasolacrimal duct: implications for congenital obstruction. Ophthalmology 2010;117:2430-34. 10. Wilson G, Merrill R. The lacrimal drainage system: pressure changes in the canaliculus. Am J Optom Physiol Opt 1976;53: 55-9. 11. Sahlin S, Chen E. Gravity, blink rate, and lacrimal drainage capacity. Am J Ophthalmol 1997;124:758-64. 12. Paulsen FP, Paulsen JI, Thale AB, Tillmann BN. Mucosa-associated lymphoid tissue in human efferent tear ducts. Virchows Arch 2000; 437:185-9. 13. Paulsen F. The human nasolacrimal ducts. Adv Anat Embryol Cell Biol 2003;170:1-106. 14. Kusters MA, Verstegen RH, Gemen EF, de Vries E. Intrinsic defect of the immune system in children with Down syndrome: a review. Clin Exp Immunol 2009;156:189-93. 15. Bloemers BL, van Bleek GM, Kimpen JL, Bont L. Distinct abnormalities in the innate immune system of children with Down syndrome. J Pediatr 2010;156:804-9.

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16. Doane MG. Blinking and the mechanics of the lacrimal drainage system. Ophthalmology 1981;88:844-51. 17. Jones LT. An anatomical approach to problems of the eyelids and lacrimal apparatus. Arch Ophthalmol 1961;66:111-24. 18. Jones LT. Epiphora: II. Its relation to the anatomic structures and surgery of the medial canthal region. Am J Ophthalmol 1957;43: 203-12. 19. Becker BB. Tricompartment model of the lacrimal pump mechanism. Ophthalmology 1992;99:1139-45. 20. Paulsen FP, Thale AB, Hallmann UJ, Schaudig U, Tillmann BN. The cavernous body of the human efferent tear ducts: function in tear outflow mechanism. Invest Ophthalmol Vis Sci 2000;41:965-70. 21. Mills DM, Tsai S, Meyer DR, Belden C. Pediatric ophthalmic computed tomographic scanning and associated cancer risk. Am J Ophthalmol 2006;142:1046-53. 22. Brenner DJ, Elliston CD, Hall EJ, Berdon WE. Estimates of the cancer risks from pediatric CT radiation are not merely theoretical: comment on “point/counterpoint: in x-ray computed tomography, technique factors should be selected appropriate to patient size against the proposition.”. Med Phys 2001;28:2387-8. 23. Udayasankar UK, Braithwaite K, Arvaniti M, et al. Low-dose nonenhanced head CT protocol for follow-up evaluation of children with ventriculoperitoneal shunt: reduction of radiation and effect on image quality. AJNR Am J Neuroradiol 2008;29:802-6.

First Person

A 5-year-old asked me in clinic today if he was going to get his eyes “annihilated” [dilated!]. Contributed by Todd Goldblum, MD, Albuquerque, New Mexico

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