The "Risser+" grade: a new grading system to classify skeletal maturity in idiopathic scoliosis.

PURPOSE: This study aims to propose and validate a new unified "Risser+" grade that combines the North American (NA) and European (EU) variants of the classic Risser score. The "Risser+ " grade can effectively combine the North American and European Risser Classifications for skeletal maturity with adequate intra-rater/inter-rater reliability and agreement. METHODS: Agreement and reliability were evaluated for 6 raters (3-NA, 3-EU) who assessed 120 pelvic radiographs from the BrAIST trial, all female, average age 13.4 (range 10.1-16.5 years). Blinded raters reviewed x-rays at two time-points. Intra- and inter-rater agreement (RA) were established with Krippendorff's alpha (k-alpha), while intra- and inter-rater reliability (RR) were established with intraclass correlation coefficients (ICC). Acceptable agreement and reliability were set a priori at 0.80. RESULTS: Inter-RA for the second reading met study requirements (k-alpha = 0.86 [0.81-0.90]) compared to the first reading (0.72 [0.63-0.79]) while combined readings was close to target agreement (0.79 [0.74-0.84]). Removal of 20 readings demonstrating outlier tendencies increased agreement for the first, second, and combined reads (k-alpha = 0.85, 0.89, 0.87, respectively). Intra-RA was sufficient for 4 out of 6 raters (k-alpha > 0.80) and one rater from EU and NA presented subpar intra-RA (k-alpha = 0.64 and 0.74, respectively). Inter-RR met study requirements overall reads (ICC = 0.96 [0.95-0.97]) including the first (0.94 [0.92-0.95]) and second (0.97 [0.97-0.98]) reads, independently. CONCLUSIONS: The Risser+ system showed excellent reliability across multiple reads and raters and demonstrated 79% agreement overall reads and ratings. Agreement increased to over 85% when raters could distinguish Risser 0 + from Risser 5. These slides can be retrieved from electronic supplementary material.

Correction to: The "Risser+" grade: a new grading system to classify skeletal maturity in idiopathic scoliosis.

Unfortunately, the affiliation of the author Negrini S has been incorrectly published in the original version. The complete correct affiliation of this author should read as follows.

Particle damage sources for fused silica optics and their mitigation on high energy laser systems.

High energy laser systems are ultimately limited by laser-induced damage to their critical components. This is especially true of damage to critical fused silica optics, which grows rapidly upon exposure to additional laser pulses. Much progress has been made in eliminating damage precursors in as-processed fused silica optics (the advanced mitigation process, AMP3), and very high damage resistance has been demonstrated in laboratory studies. However, the full potential of these improvements has not yet been realized in actual laser systems. In this work, we explore the importance of additional damage sources-in particular, particle contamination-for fused silica optics fielded in a high-performance laser environment, the National Ignition Facility (NIF) laser system. We demonstrate that the most dangerous sources of particle contamination in a system-level environment are laser-driven particle sources. In the specific case of the NIF laser, we have identified the two important particle sources which account for nearly all the damage observed on AMP3 optics during full laser operation and present mitigations for these particle sources. Finally, with the elimination of these laser-driven particle sources, we demonstrate essentially damage free operation of AMP3 fused silica for ten large optics (a total of 12,000 cm2 of beam area) for shots from 8.6 J/cm2 to 9.5 J/cm2 of 351 nm light (3 ns Gaussian pulse shapes). Potentially many other pulsed high energy laser systems have similar particle sources, and given the insight provided by this study, their identification and elimination should be possible. The mitigations demonstrated here are currently being employed for all large UV silica optics on the National Ignition Facility.

Mitigation of organic laser damage precursors from chemical processing of fused silica.

Increases in the laser damage threshold of fused silica have been driven by the successive elimination of near-surface damage precursors such as polishing residue, fractures, and inorganic salts. In this work, we show that trace impurities in ultrapure water used to process fused silica optics may be responsible for the formation of carbonaceous deposits. We use surrogate materials to show that organic compounds precipitated onto fused silica surfaces form discrete damage precursors. Following a standard etching process, solvent-free oxidative decomposition using oxygen plasma or high-temperature thermal treatments in air reduced the total density of damage precursors to as low as <50 cm(-2). Finally, we show that inorganic compounds are more likely to cause damage when they are tightly adhered to a surface, which may explain why high-temperature thermal treatments have been historically unsuccessful at removing extrinsic damage precursors from fused silica.

Fracture-induced subbandgap absorption as a precursor to optical damage on fused silica surfaces.

The optical damage threshold of indentation-induced flaws on fused silica surfaces was explored. Mechanical flaws were characterized by laser damage testing, as well as by optical, secondary electron, and photoluminescence microscopy. Localized polishing, chemical leaching, and the control of indentation morphology were used to isolate the structural features that limit optical damage. A thin defect layer on fracture surfaces, including those smaller than the wavelength of visible light, was found to be the dominant source of laser damage initiation during illumination with 355 nm, 3 ns laser pulses. Little evidence was found that either displaced or densified material or fluence intensification plays a significant role in optical damage at fluences >35 J/cm(2). Elimination of the defect layer was shown to increase the overall damage performance of fused silica optics.

Pancreatic secretion by nonparallel exocytosis: potential resolution of a long controversy.

The idea that pancreatic digestive enzyme secretion can occur in a nonparallel manner has been controversial because of its presumed incompatibility with the exocytosis secretory mechanism. Correlation and regression analysis of enzyme output by the rabbit pancreas after it is stimulated with cholecystokinin and chymodenin revealed that digestive enzymes are secreted in a highly linked fashion, compatible with exocytosis and with nonparallel secretion. Thus, exocytosis and nonparallel secretion are not contradictory processes, but rather nonparallel secretion is due to exocytosis from heterogeneous sources within the pancreas.

Prospective evaluation of parental anxiety related to newborn foot disorder.

PURPOSE: The presence of a clubfoot is often found prenatally and some families seek counselling with a specialist. The purpose of this study was to compare the parental anxiety levels in families that: a) knew prenatally and had prenatal counselling; b) knew prenatally but did not seek prenatal counselling; and c) did not know until after delivery. METHODS: This prospective cohort study evaluated the anxiety of parents as they presented to the paediatric orthopaedic clinic with their newborn with a foot disorder (prior to the diagnostic confirmation of clubfoot). Each family filled out the 'Pre-visit orthopaedic surgeon questionnaire' and then after the initial visit with the orthopaedic surgeon (confirming the clubfoot diagnosis) the family filled out the 'Immediately post-visit orthopaedic surgeon questionnaire'. Through these questionnaires, anxiety level was assessed prior to meeting postnatally with the paediatric orthopaedic specialist, as well as after the meeting and compared across groups. RESULTS: A total of 121 parents completed questionnaires: 71% (86/121) confirmed clubfoot; 69% of families (59/86) received prenatal counselling (Group A); 16% (14/86) knew prenatally but had no counselling (Group B); and 15% (13/86) found out at birth (Group C). There was no difference in anxiety levels across groups before (p = 0.78) or after (p = 0.57) meeting with the paediatric orthopaedic surgeon; however, overall anxiety reduced significantly (p < 0.001). CONCLUSION: We found no difference in the anxiety levels of across the three groups. Prenatal counselling for parents of children with likely clubfoot may not decrease parental anxiety, but nonetheless is very appreciated by the families who receive it. LEVEL OF EVIDENCE: Prognostic Level II.

Age- and gender-specific variations of the epiphyseal tilt and epiphyseal angle in adolescents without hip pathology.

PURPOSE: To determine age-and gender-dependent variation of epiphyseal tilt and epiphyseal angle using CT in adolescents without hip pathology. METHODS: Pelvic CT scans were obtained in 132 adolescents for evaluation of abdominal pain. Radially oriented planes around the femoral neck were reformatted and the epiphyseal tilt and angle were measured in the anterior, anterosuperior and superior planes. Variations in the tilt angle and epiphyseal angle were assessed by age group from 12 to 18 years and gender by using a linear mixed model analysis. RESULTS: The epiphyseal tilt did not change (p = 0.97) with increasing age. Male patients exhibited smaller tilt angle in the anterosuperior plane (p = 0.003) but no difference was detected in the anterior (p = 0.17) or superior (p = 0.06) planes. The epiphyseal angle decreased with increasing age in the anterior (p = 0.03), anterosuperior (p = 0.001) and superior (p < 0.001) planes in male patients, with no variation in female patients (p = 0.92). Male patients had larger epiphyseal angles in the anterior (p = 0.02), anterosuperior (p < 0.001) and superior (p = 0.002) planes compared with female patients. CONCLUSION: We found no age-specific variations in the epiphyseal tilt and no difference in the epiphyseal tilt in male and female patients in the superior and anterior plane. The epiphyseal angle was smaller in female patients, however, the epiphyseal angle decreased with increasing age in male patients which corresponds to an increase in epiphyseal extension. The reference values reported in this study may serve as additional information in the evaluation of adolescents with hip pain and as reference for future studies investigating slipped capital femoral epiphysis and femoroacetabular impingement development. LEVEL OF EVIDENCE: Level III Diagnostic Study.

Acetabular morphology in slipped capital femoral epiphysis: comparison at treatment onset and skeletal maturity.

PURPOSE: To investigate changes in acetabular morphology during the follow-up of slipped capital femoral epiphysis (SCFE) and search for factors associated with acetabular dysplasia at skeletal maturity. METHODS: We evaluated 108 patients with unilateral SCFE (mean age at slip, 12.3 years sd 1.7) to skeletal maturity, with a minimum follow-up of two years (median 4.5 years; interquartile range 3.2 to 6.2). Acetabular parameters obtained from initial and most recent radiographs included the lateral centre-edge angle (LCEA), Tönnis angle (TA) and acetabular depth-width ratio (ADR). Acetabular dysplasia was considered for LCEA < 20° or TA > 10°. Femoral parameters consisted of the most recent head diameter, neck-shaft angle, neck length, articulotrochanteric distance and alpha angle. RESULTS: At SCFE onset, the affected hip showed a slightly lower LCEA (26.4° sd 6.1° versus 27.3° sd 5.7°; p = 0.01) and ADR (330 sd 30 versus 340 sd 30; p < 0.001) compared with the uninvolved hip. At final follow-up, the affected hip showed lower LCEA (24.5° sd 7.6° versus 28.8°sd 6.6°; p < 0.001) and ADR (330 sd 40 versus 350 sd 40; p < 0.001), and TA was larger (5.5° sd 5.4° versus 2.3° sd 4.2°; p < 0.001) compared with the uninvolved hip. Acetabular dysplasia was observed in 27 (25%) of 108 hips with SCFE. Femoral head overgrowth, age at slip and SCFE severity were independent factors associated with acetabular dysplasia (p < 0.05). CONCLUSION: Acetabular coverage and depth are not increased in SCFE, and the acetabular coverage tends to decrease up to skeletal maturity. A potential disturbance in the acetabular growth and remodelling exists mainly for young children with severe SCFE, and a potential for acetabular insufficiency may be observed at the diagnosis and follow-up of SCFE. LEVEL OF EVIDENCE: Prognostic Level IV.

Syndesmosis injuries in the pediatric and adolescent athlete: an analysis of risk factors related to operative intervention.

PURPOSE: To review all paediatric ankle syndesmotic injuries occurring at our institution and identify risk factors associated with operative intervention. METHODS: Among 22 873 evaluations for ankle trauma, we found 220 children suffering from syndesmotic injuries (incidence: 0.96%). We recorded demographic data, details of the injury, features on examination and treatment variables. Univariable and multivariable logistic regression modelling was performed to identify risk factors associated with operative intervention. RESULTS: The mean age at injury was 15.8 years (8.9 to 19.0) with a median follow-up of 13 weeks (IQR 5 to 30 weeks). A sports-related injury was most common (168/220, 76%). A total of 82 of 220 (37%) patients underwent operative fixation, of which 76 (93%) had an associated fibular fracture. Patients undergoing surgery had a higher incidence of swelling and inability to weight bear (p < 0.001). Statistically significant differences were recorded in tibiofibular (TF) clear space, TF overlap and medial clear space (MCS) between the operative and non-operative cohorts (6.0 vs 4.6 mm (p = 0.002), 5.4 vs 6.9 mm (p = 0.004) and 6.4 vs 3.5 mm (p < 0.001)). Multivariable analysis revealed patients with a fracture of the ankle had 44 times the odds of surgical intervention, patients with a closed physis had over five times the odds of surgical intervention and patients with a medial clear space greater than 5 mm had nearly eight times the odds of requiring surgical intervention. CONCLUSIONS: Operative ankle syndesmotic injuries in the paediatric population are often associated with a closed distal tibial physis and concomitant fibular fracture.

Effects of 0.2% brimonidine and 0.2% brimonidine-0.5% timolol on intraocular pressure and pupil size in normal equine eyes.

BACKGROUND: Brimonidine is an α2 -adrenergic agonist that decreases aqueous humour production and may increase uveoscleral outflow. It has not been evaluated in normal or glaucomatous equine eyes. OBJECTIVES: To evaluate the efficacy and safety of brimonidine in lowering intraocular pressure (IOP), alone and in conjunction with timolol, as a treatment for equine glaucoma by comparing IOP in normal equine eyes treated with brimonidine and brimonidine-timolol, respectively, with IOP in control eyes. STUDY DESIGN: A balanced crossover design with 16 horses receiving one of two treatments, brimonidine and brimonidine-timolol, during each of two 10-day study phases, was used. Four horses were randomly assigned to each of four combinations of treated eye (right or left) and drug order within the two 10-day study phases (brimonidine first or brimonidine-timolol first). METHODS: Pupil size and conjunctival hyperaemia were assessed twice per day and IOP was measured three times per day using rebound tonometry in both eyes of 16 normal horses throughout two 10-day study periods (brimonidine and brimonidine-timolol) separated by an 18-day washout period. One eye of each horse was treated with brimonidine or brimonidine-timolol and the opposite eye was treated with balanced salt solution (BSS). RESULTS: There were no adverse effects and no significant changes in pupil size in normal equine eyes treated with brimonidine or brimonidine-timolol. Average IOP in normal equine eyes treated with brimonidine (25.6 mmHg) was statistically higher than in eyes treated with brimonidine-timolol (24.6 mmHg) or BSS (24.5 mmHg). However, IOP differences were of ≤1 mmHg and thus not clinically important. MAIN LIMITATIONS: Horses with normal eyes may not be as sensitive to the IOP-lowering effects of treatment as horses with glaucoma. CONCLUSIONS: Brimonidine and brimonidine-timolol are well tolerated in normal horses but do not decrease IOP.

erbB-2 oncogene inhibition by geldanamycin derivatives: synthesis, mechanism of action, and structure-activity relationships.

Overexpression of the erbB-2 oncogene has been linked to poor prognosis in breast, ovarian, and gastric cancers. Naturally occurring benzoquinoid ansamycin antibiotics herbimycin A, geldanamycin (GDM), and dihydrogeldanamycin were found to potently deplete p185, the erbB-2 oncoprotein, in human breast cancer SKBR-3 cells in culture. Chemistry efforts to modify selectively the ansa ring of GDM afforded derivatives with greater potency in vitro and in vivo. Analogs demonstrated inhibition of p185 phosphotyrosine in cell culture and in vivo after systemic drug administration to nu/nu nude mice bearing Fisher rat embryo cells transfected with human erbB-2. Functional group modification in the ansa ring was performed stereoselectively and regiospecifically without the need for protection strategies. Essential functional groups that were required for anti-erbB-2 activity were the 7-carbamate and the 2,3-double bond. Modification of the functional groups at the other positions was permitted. Structure-activity relationships are described for 1-5-, 7-9-, 11-, 15-, and 22-substituted geldanamycins.

Distribution of microtubule-associated protein 2 in the nervous system of the rat studied by immunofluorescence.

It has recently been reported that high molecular weight microtubule-associated proteins are differently distributed in dendrites and axons of neurons [ Matus Bernhardt and Hugh-Jones (1981), Proc. natn Acad. Sci. U.S.A. 78, 3010-3014; Vallee (1982), J. Cell Biol. 92, 435-442]. We have reported earlier in a preliminary form [Miller, Walter, Theurkauf , Vallee and De Camilli (1982), Proc. natn Acad. Sci. U.S.A. 79, 5562-5566] that an antiserum specific for microtubule-associated protein 2, one of the most prominent high molecular weight microtubule-associated proteins in brain and a major brain phosphoprotein, stains specifically neuronal dendrites and perikarya. We have now extended those observations by performing a detailed analysis of the distribution of microtubule-associated protein 2 throughout the nervous system of the rat. We found that microtubule-associated protein 2 is present at high concentrations in the great majority of neurons. Under our conditions of immunostaining microtubule-associated protein 2 was not detected in nonneuronal cells. In all neurons it was compartmentalized in perikarya and dendrites. In most cases, the latter were more heavily stained than perikarya. The pattern of staining (overall intensity, relative intensity in dendrites vs perikarya, and in proximal vs distal segments of the dendritic tree), varied in different classes of neurons but was identical for all neurons with similar geometry in the same brain region. Different patterns of staining were found in dendritic trees with dissimilar branching characteristics. In all cases staining for microtubule-associated protein 2 in dendrites was consistent with a localization of microtubule-associated protein 2 on dendritic microtubules. Neuronal processes clearly identifiable as axons or axon terminals were not immunostained. Afferent processes of primary sensory cells were also unstained. Our findings indicate that microtubule-associated protein 2 is a component of the vast majority, and possibly all, neurons. It is highly concentrated in "bona fide" dendrites, i.e. in processes specialized for the reception of synaptic inputs on their surface and highly dependent on such inputs for their growth. The location of microtubule-associated protein 2, a major target for second messenger-regulated protein kinases, in these processes, supports the hypothesis that its phosphorylation might participate in the transduction of neurotransmitter signals in target nerve cells.

Anatomy of cerebellar Purkinje cells in the rat determined by a specific immunohistochemical marker.

In the present study we have used guanosine 3':5'-phosphate-dependent protein kinase antiserum, a specific immunohistochemical marker for cerebellar Purkinje cells, [ Lohmann , Walter, Miller, Greengard and De Camilli (1981) Proc. natn . Acad. Sci. U.S.A. 78, 653-657], to carry out a detailed analysis of the architecture and projections of Purkinje cells in the adult rat. We have obtained a novel view of aspects of Purkinje cell morphology that were already known and, in addition, we have provided some new information, in particular on the targets of Purkinje cell axons and their pattern of innervation, and on the morphology and course of Purkinje cell axons. Furthermore, we have found a few cells positive for guanosine 3':5' phosphate-dependent protein kinase which are very similar morphologically to Purkinje cells but are located outside of the cerebellar cortex. A unique feature of Purkinje cells is their peculiar monoplanar shape. Not only do their dendritic arbors lie in planes perpendicular to the major axis of the folia, but their axons, including the collaterals, also travel roughly in the same planes. Thus, Purkinje cells can be imagined as lying in longitudinal sheets radiating from the deep cerebellar nuclei. In these sheets, Purkinje cell axons originating from cells located at different rostrocaudal levels of the cortex converge towards the deep cerebellar nuclei without intersecting each other. It is as a result of this precise organization that Purkinje cell axons reach the deep cerebellar nuclei with a mediolateral and rostrocaudal topology that closely reflects the position of their parent cells in the cerebellar cortex. In the subcortical rays of white matter, Purkinje cell axons are interspersed with other axons, being excluded only from longitudinal strips which correspond to the cerebellar raphes . Upon converging towards the deep cerebellar nuclei they segregate into tracts of white matter that alternate with tracts of white matter from which they are excluded. The great majority of Purkinje cell axons terminate in the deep cerebellar nuclei. Recurrent collaterals terminate in close proximity to the Purkinje cell layer. Dense innervation by these axons is found around large interneurons ( Lugaro and Golgi cells) and around the Purkinje cell pinceaux . No direct input of recurrent collaterals to Purkinje cell somata is evident in immunostained material. A substantial number of Purkinje cell axons continue beyond the cerebellar nuclei to innervate nearby regions in the brain stem.(ABSTRACT TRUNCATED AT 400 WORDS)

Natural history of arteriovenous grafts in hemodialysis patients.

Most hemodialysis patients in the United States have an arteriovenous graft as their vascular access. Grafts have a relatively short life span and are prone to recurrent stenosis and thrombosis, requiring multiple salvage procedures to maintain their patency. There is little information in the literature regarding the clinical factors that determine graft survival and complications. We evaluated prospectively the outcomes of 256 grafts placed at a single institution during a 2-year period. A salvage procedure to maintain graft patency (thrombectomy, angioplasty, or surgical revision) was required in 29% of the grafts at 3 months, 52% at 6 months, 77% at 12 months, and 96% at 24 months. Thus, primary graft survival (time from graft placement to the first intervention) was only 23% at 1 year and 4% at 2 years. Primary graft survival was significantly less among patients with hypoalbuminemia compared with patients with a normal serum albumin level (P = 0.003). Secondary graft survival (time from graft placement to permanent graft failure) was 65% at 1 year and 51% at 2 years. Neither primary nor secondary graft survival was significantly correlated with patient age, sex, diabetic status, body mass index, or graft site. A mean of 1.22 interventions per graft-year were required to maintain access patency, including 0.51 thrombectomies, 0.54 angioplasties, and 0.17 surgical revisions. In conclusion, hypoalbuminemia is a strong predictor of the requirement for an early graft intervention. Patients with hypoalbuminemia may require a heightened index of suspicion in monitoring their grafts for evidence of stenosis.

Perioperative spinal canal narrowing in patients with Down's syndrome.

Two patients with Down's syndrome undergoing intracardiac operations had segmental and generalized myoclonic movements postoperatively and eventual brain death. Electroencephalography in 1 patient showed no seizure despite the presence of the myoclonic movements. Computed tomographic scan showed possible cerebellar hemorrhage. Ultrasound showed cerebral edema when the pupils became fixed and dilated. Because known postoperative neurologic complications could not fully explain the clinical course, and the myoclonic movements suggested spinal origin, we considered the possibility of atlantoaxial instability causing spinal cord damage related to perioperative head and neck positioning. Postmortem study on the second patient revealed 50% reduction of the spinal canal with hyperextension and 90-degree external rotation of the head and neck. In contrast, similar maneuvers in 3 infants without Down's syndrome resulted in only mild spinal canal narrowing. Although the myoclonic movements could be explained by spinal cord compression at the atlantoaxial level, the explanation for the eventual brain death is unclear. However, kinking of the vertebral arteries related to the positioning could have caused cerebellar ischemia, hemorrhage, and increased intracranial pressure. We believe that attention to the problem might bring further answers in the future.

Effects of topical administration of 0.5% apraclonidine on intraocular pressure, pupil size, and heart rate in clinically normal cats.

OBJECTIVE: To evaluate the effect of a topical alpha 2-agonist, 0.5% apraclonidine, on intraocular pressure (IOP), pupil size, and heart rate in clinically normal cats. DESIGN: Randomized masked saline-controlled case study. ANIMALS: Nine clinically normal conditioned adult cats of either sex. PROCEDURE: Normal diurnal variation in IOP, pupil size, and resting heart rate was determined from 7 AM to 7 PM (day 1). On day 2, the same measurements were made after the topical application of 30 microliters of 0.5% apraclonidine to 1 randomly chosen eye of each cat. The contralateral eye received saline solution. RESULTS: Apraclonidine lowered IOP a mean of 4.8 mm of Hg (24.0%) when compared with IOP in the fellow saline-treated eye 6 hours after treatment. Unilateral administration of the drug also may have reduced IOP in both eyes. Pupil size was reduced a mean 46% in only the apraclonidine-treated eye, and miosis persisted for up to 24 hours. Heart rate was significantly lower (11.8%) at 3 hours, and 8 of 9 cats vomited after topical administration of the drug. Mild blanching of the conjunctiva occurred in all apraclonidine-treated eyes. CONCLUSIONS: Apraclonidine reduced IOP, pupil size, and resting heart rate in clinically normal cats, but also induced undesirable systemic side-effects. In contrast to dogs where the drug induced mydriasis, apraclonidine caused miosis in cats. CLINICAL RELEVANCE: The current commercially available formulation of topical 0.5% apraclonidine is too toxic for clinical use in cats. Reformulation, or identification of a less toxic congener, may result in a clinically useful antiglaucoma preparation for cats.

Effects of experimentally induced hypothyroidism on the eye and ocular adnexa of dogs.

Schirmer tear test (STT), intraocular pressure (IOP) measurement, slit-lamp biomicroscopy, and indirect ophthalmoscopy were performed on 8 dogs with 131I-induced hypothyroidism and 4 euthyroid control dogs at weeks 0, 9, 13, 17, immediately prior to treatment with levothyroxine, after 5 weeks of levothyroxine administration (0.022 mg/kg of body weight, PO, q 12 h), and at euthanasia 7 weeks after discontinuation of replacement therapy. Although the control group had higher baseline STT values than the hypothyroid group after randomization of dogs into the 2 groups (P < 0.01), STT values remained unchanged from their respective baseline values at all time intervals for both groups. Hypothyroid and control dogs had significant (P < 0.05) reduction in IOP from baseline values at all subsequent time points, but differences were not observed when hypothyroid dogs were compared with controls. Goblet cell indices determined from biopsy samples of the inferior-nasal conjunctival fornix obtained before induction of hypothyroidism (baseline), immediately prior to and at conclusion of levothyroxine therapy, and at euthanasia were not significantly different when values for hypothyroid dogs were compared with their own baseline values or with values for control dogs. Histologic examination of the globes and adnexa at euthanasia also failed to indicate consistent qualitative differences between hypothyroid and control dogs. Marked reduction in serum thyroid hormone concentrations had little effect on the eye and ocular adnexa over the course of the study.

Intraocular pressure measurement through two types of plano therapeutic soft contact lenses in dogs.

Intraocular pressure (IOP) was measured by use of Mackay-Marg applanation tonometry in 8 normal, manometrically controlled, enucleated, canine eyes with and without 1 of 2 plano therapeutic soft contact lenses (1 and 2) covering the cornea. Differences were not significant between measurements made without a contact lens and those made through either lens at manometer IOP < 30 mm of Hg. At manometer IOP > or = 30 mm of Hg, use of a contact lens tended to result in a statistically greater (P < 0.05) estimate of IOP than when a lens was not used. This difference, however, achieved only a maximum of 2.6 mm of Hg at the 80 mm of Hg value, and was not regarded as clinically important. Measurements obtained through lens 1 were not significantly different from those obtained through lens 2. The IOP can be accurately estimated in dogs, using the Mackay-Marg tonometer, without removing either type of bandage soft contact lens, thereby avoiding potential disruption of an already compromised cornea.

Effects of topical administration of 0.5% apraclonidine on intraocular pressure, pupil size, and heart rate in clinically normal dogs.

OBJECTIVE: To evaluate the effect of 0.5% apraclonidine on intraocular pressure (IOP), pupil size, and heart rate in clinically normal dogs. DESIGN: Randomized masked saline-controlled case study. ANIMALS: Nine clinically normal conditioned adult dogs of either sex. PROCEDURE: Normal diurnal variation in IOP, pupil size, and resting heart rate were determined from 7 AM to 7 PM (day 1). These measurements were repeated on day 2 after topical application of 60 microliters of 0.5% apraclonidine to 1 randomly chosen eye of each dog. The contralateral eye received saline solution. RESULTS: Compared with the saline-treated fellow eye, mean IOP in the apraclonidine-treated eye was significantly reduced (3.0 mm of Hg, 16%) 8 hours after treatment. Because of mild day-to-day variations in IOP, however, IOP in the apraclonidine-treated eye on day 2 was not significantly different from day-1 baseline values obtained from the same eye. Significant mydriasis (2.1 mm, 29.7%), persisting for up to 8 hours, occurred in apraclonidine-treated eyes. Although apraclonidine did not significantly alter heart rate when all 9 dogs were viewed as a group, 4 dogs experienced a 9 to 19.5% reduction in heart rate 2 hours after treatment. Mild blanching of the conjunctiva occurred in apraclonidine-treated eyes. CONCLUSIONS: Apraclonidine lowered IOP and, in contrast to cats where it causes miosis, induced mydriasis in dogs. Although heart rate generally is unchanged, it may be reduced in select individuals. CLINICAL RELEVANCE: Topically applied 0.5% apraclonidine may be a useful adjunct to other antiglaucoma treatment modalities in dogs, but is unlikely to be effective as the sole agent in most forms of canine glaucoma.