Basal Tear Osmolarity as a metric to estimate body hydration and dry eye severity.

The osmolarities of various bodily fluids, including tears, saliva and urine, have been used as indices of plasma osmolality, a measure of body hydration, while tear osmolarity is used routinely in dry eye diagnosis, the degree of tear hyperosmolarity providing an index of disease severity. Systemic dehydration, due to inadequate water intake or excessive water loss is common in the elderly population, has a high morbidity and may cause loss of life. Its diagnosis is often overlooked and there is a need to develop a simple, bedside test to detect dehydration in this population. We hypothesize that, in the absence of tear evaporation and with continued secretion, mixing and drainage of tears, tear osmolarity falls to a basal level that is closer to that of the plasma than that of a tear sample taken in open eye conditions. We term this value the Basal Tear Osmolarity (BTO) and propose that it may be measured in tear samples immediately after a period of evaporative suppression. This value will be particular to an individual and since plasma osmolarity is controlled within narrow limits, it is predicted that it will be stable and have a small variance. It is proposed that the BTO, measured immediately after a defined period of eye closure, can provide a new metric in the diagnosis of systemic dehydration and a yardstick against which to gauge the severity of dry eye disease.

Clinical staining of the ocular surface: mechanisms and interpretations.

In this article we review the mechanism of ocular surface staining. Water-soluble dyes are excluded from the normal epithelium by tight junctions, the plasma membranes and the surface glycocalyx. Shed cells can take up dye. A proportion of normal corneas show sparse, scattered time-dependent, punctate fluorescein uptake, which, we hypothesise, is due to a graded loss of the glycocalyx barrier, permitting transcellular entry into pre-shed cells. In pathological staining, there is little evidence of 'micropooling' at sites of shedding and the term 'punctate erosion' may be a misnomer. It is more likely that the initial event involves transcellular dye entry and, in addition, diffusion across defective tight junctions. Different dye-staining characteristics probably reflect differences in molecular size and other physical properties of each dye, coupled with differences in visibility under the conditions of illumination used. This is most relevant to the rapid epithelial spread of fluorescein from sites of punctate staining, compared to the apparent confinement of dyes to staining cells with dyes such as lissamine green and rose bengal. We assume that fluorescein, with its lower molecular weight, spreads initially by a paracellular route and then by transcellular diffusion. Solution-Induced Corneal Staining (SICS), related to the use of certain contact lens care solutions, may have a different basis, involving the non-pathological uptake of cationic preservatives, such as biguanides, into epithelial membranes and secondary binding of the fluorescein anion. It is transient and may not imply corneal toxicity. Understanding the mechanism of staining is relevant to the standardisation of grading, to monitoring disease and to the conduct of clinical trials.

The ageing lens and cataract: a model of normal and pathological ageing.

Cataract is a visible opacity in the lens substance, which, when located on the visual axis, leads to visual loss. Age-related cataract is a cause of blindness on a global scale involving genetic and environmental influences. With ageing, lens proteins undergo non-enzymatic, post-translational modification and the accumulation of fluorescent chromophores, increasing susceptibility to oxidation and cross-linking and increased light-scatter. Because the human lens grows throughout life, the lens core is exposed for a longer period to such influences and the risk of oxidative damage increases in the fourth decade when a barrier to the transport of glutathione forms around the lens nucleus. Consequently, as the lens ages, its transparency falls and the nucleus becomes more rigid, resisting the change in shape necessary for accommodation. This is the basis of presbyopia. In some individuals, the steady accumulation of chromophores and complex, insoluble crystallin aggregates in the lens nucleus leads to the formation of a brown nuclear cataract. The process is homogeneous and the affected lens fibres retain their gross morphology. Cortical opacities are due to changes in membrane permeability and enzyme function and shear-stress damage to lens fibres with continued accommodative effort. Unlike nuclear cataract, progression is intermittent, stepwise and non-uniform.

Role of keratan sulphate (sulphated poly -N-acetyllactosamine repeats) in keratoconic cornea, histochemical, and ultrastructural analysis.

AIMS: Keratan sulphate (KS) is the predominant glycosaminoglycan (GAG) present in the corneal stroma where it is thought to regulate collagen fibril diameter. In this study we investigated the distribution of KS in normal and keratoconic corneas. METHODS: Four normal, one mild, and four severe keratoconic corneas were used for the study. Distribution of keratan sulphate proteoglycans (KS-PG) was investigated using a primary monoclonal antibody (5-D-4) that recognizes disulphated disaccharides in the poly-N-acetyllactosamine repeats of KS. The immuno-reactivity of 5-D-4 was analyzed by immunohistochemistry and immuno-electron microscopy. RESULTS: Immuno-histochemistry showed diffuse 5-D-4 staining in keratoconic cornea compared to the punctuate staining in normal corneas. In the single cornea with mild keratoconus, immunogold microscopy revealed a very high density of KS-PG staining, especially in the posterior stroma, compared to severe keratoconic and normal cornea. The amount of KS-PG in the stroma in severe keratoconus was slightly less compared to the normal cornea. In the mild keratoconic cornea, a higher quantity of KS-PG was present around the keratocytes. In severe keratoconic corneas, a higher quantity of KS-PG was present within the keratocytes compared to normal cornea. CONCLUSIONS: The finding of an altered expression of KS in our keratoconic corneas, in particular the strong expression of KS in keratocytes, is in keeping with reports of an altered expression of proteoglycan metabolism in keratoconus. KS-PG plays an important role in stromal collagen fibril assembly and a dysregulation of KS-PG synthesis or catabolism could explain changes in collagen fibril spacing and diameter, which we have reported elsewhere.

A mass and solute balance model for tear volume and osmolarity in the normal and the dry eye.

Tear hyperosmolarity is thought to play a key role in the mechanism of dry eye, a common symptomatic condition accompanied by visual disturbance, tear film instability, inflammation and damage to the ocular surface. We have constructed a model for the mass and solute balance of the tears, with parameter estimation based on extensive data from the literature which permits the influence of tear evaporation, lacrimal flux and blink rate on tear osmolarity to be explored. In particular the nature of compensatory events has been estimated in aqueous-deficient (ADDE) and evaporative (EDE) dry eye. The model reproduces observed osmolarities of the tear meniscus for the healthy eye and predicts a higher concentration in the tear film than meniscus in normal and dry eye states. The differential is small in the normal eye, but is significantly increased in dry eye, especially for the simultaneous presence of high meniscus concentration and low meniscus radius. This may influence the interpretation of osmolarity values obtained from meniscus samples since they need not fully reflect potential damage to the ocular surface caused by tear film hyperosmolarity. Interrogation of the model suggests that increases in blink rate may play a limited role in compensating for a rise in tear osmolarity in ADDE but that an increase in lacrimal flux, together with an increase in blink rate, may delay the development of hyperosmolarity in EDE. Nonetheless, it is predicted that tear osmolarity may rise to much higher levels in EDE than ADDE before the onset of tear film breakup, in the absence of events at the ocular surface which would independently compromise tear film stability. Differences in the predicted responses of the pre-ocular tears in ADDE compared to EDE or hybrid disease to defined conditions suggest that no single, empirically-accessible variable can act as a surrogate for tear film concentration and the potential for ocular surface damage. This emphasises the need to measure and integrate multiple diagnostic indicators to determine outcomes and prognosis. Modelling predictions in addition show that further studies concerning the possibility of a high lacrimal flux phenotype in EDE are likely to be profitable.

NADPH-diaphorase expression in the meibomian glands of rat palpebra in postnatal development.

In the current study, we aimed at investigating the presence of nitric oxide synthase (NOS) positive nerve fibers in rat meibomian glands (MGs) at various stages of development. There is good evidence to suggest that nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) is a surrogate for neuronal nitric oxide synthase (NOS). Sections of the central, upper eyelids of Wistar rats were processed histochemically for NADPH-d to investigate the presence and distribution of NOS-positive nerve fibers at the following time points: day 1 and weeks 1, 2 and 3 post partum, and in adult controls. At day 1, MG acini were lightly stained and located at a distance from the mucosal border. Vessels were accompanied by intensely stained NADPH-d positive nerve fibers. At the week 1 time point, both the vessels and the NADPH-d positive fibers were still present, but less numerous. MGs were now closer to the mucosa, so that the submucosa was thinner. The acini were mostly pale but occasionally darker. At week 3, there were fewer blood vessels in both the submucosa and within the septa. Darker acini were more common than lightly stained acini. NADPH-d positive dots were observed in the vicinity of the MGs. At the week 3 time point, MGs were adjacent to the mucosal border and stained more intensely than at earlier times; almost all acini were stained. The microscopic appearances were almost identical with those of adult palpebra. Submucosal and septal blood vessels and NADPH-d positive nerve fibers were less numerous. NADPH-d histochemical staining confirmed differences in the density of stained nerve fibers at different developmental stages. The greatest density of NADPH-d -positive nerve fibers occurred in 1-day-old rats whereas they were less numerous in adult rat eyelids. Nerves innervating MGs utilize nitric oxide (NO) as a neurotransmitter mostly in early developmental stages and this need thereafter decreases and stabilizes at 3 weeks postnatally.

Optic nerve sheath diameter, intracranial pressure and acute mountain sickness on Mount Everest: a longitudinal cohort study.

OBJECTIVE: To investigate the association of optic nerve sheath diameter (ONSD), as a correlate of intracranial pressure (ICP), with acute mountain sickness (AMS). DESIGN: Longitudinal cohort study of mountaineers from sea level to 6400 m. SETTING: Mount Everest (North side). PARTICIPANTS: 13 mountaineers (10 men, 3 women; aged 23-52 years) on a British expedition to climb Mount Everest. INTERVENTIONS: ONSD was measured ultrasonically, 3 mm behind the globe using B scans recorded with an OTI-Scan 3D scanner (Ophthalmic Technologies, Canada). Serial binocular scans were recorded at sea level, and 2000, 3700, 5200 and 6400 m. All ONSDs were measured by a blinded observer. MAIN OUTCOME MEASURES: ONSD, AMS score (using the Lake Louise scoring system), heart rate, and oxygen saturation levels. RESULTS: All results were analysed by regression analysis with adjustment. ONSD was positively associated with increasing altitude above sea level (0.10 mm increase in ONSD per 1000 m, 95% CI 0.05 to 0.14 mm) and AMS score (0.12 mm per score, 95% CI 0.06 to 0.18 mm); further associations were found with resting heart rate (0.29 mm per 20 beats/min, 95% CI 0.17 to 0.41 mm) and oxygen saturations (0.20 mm per 10% decrease, 95% CI 0.11 to 0.29 mm). CONCLUSIONS: ONSD increases at high altitude, and this increase is associated with more severe symptoms of AMS. Given the linkage between ONSD and ICP, these results strongly suggest that intracranial pressure plays an important role in the pathophysiology of AMS.

A hypothesis to suggest that light is a risk factor in glaucoma and the mitochondrial optic neuropathies.

The authors propose that light entering the eye interacts with retinal ganglion cell (RGC) axon mitochondria to generate reactive oxygen intermediates (ROI) and that when these neurons are in an energetically low state, their capacity to remove these damaging molecules is exceeded and their survival is compromised. They suggest that in the initial stages of glaucoma, RGCs exist at a low energy level because of a reduced blood flow at the optic nerve head and that in the mitochondrial optic neuropathies (MONs), this results from a primary, genetic defect in aerobic metabolism. In these states RGCs function at a reduced energy level and incident light on the retina becomes a risk factor. Preliminary laboratory studies support this proposition. Firstly, the authors have shown that light is detrimental to isolated mitochondria in an intensity dependent manner. Secondly, light triggers apoptosis of cultured, transformed RGCs and this effect is exacerbated when the cells are nutritionally deprived. Detailed studies are under way to strengthen the proposed theory. On the basis of this proposal, the authors suggest that patients with optic neuropathies such as glaucoma or at risk of developing a MON may benefit from the use of spectral filters and reducing the intensity of light entering the eye.

Gelatinous drop-like corneal dystrophy in a child with developmental delay: clinicopathological features and exclusion of the M1S1 gene.

AIMS: Gelatinous drop-like corneal dystrophy (GDLD) is an early-onset, autosomal recessive condition characterised by amyloid deposits within the cornea. We report the histopathological and molecular genetic findings in a Caucasian child with GDLD who also exhibited global developmental delay. METHODS: Bilateral lamellar keratoplasty was carried out at age 6 and 7 years. Tissue was fixed for light and electron microscopy, including immunoelectronmicroscopy. The coding region of the M1S1 gene was screened for mutations in the affected proband and available relatives, using DNA extracted from mouthwashes. RESULTS: Nodular deposits, which were present subepithelially and in the central superficial stroma, stained typically for amyloid with PAS and Congo red. A nodular deposit of amyloid, together with large amounts of lactoferrin and sparse amounts of keratoepithelin (betaig-h3), was present in the central superficial stroma, causing destruction of Bowman's layer and elevation of the thinned, degenerate epithelium. Around the deposit zone, the stroma exhibited large numbers of thick filamentous proteoglycan deposits. While the affected child was homozygous for a novel A1133 C single-nucleotide polymorphism (SNP) that resulted in an aspartic acid to alanine substitution at position 173 of the M1S1 coding sequence, this polymorphism was also found at relatively high frequency in a sample of normal controls, enabling exclusion of the M1S1 gene as the disease locus. CONCLUSION: Increased epithelial permeability in GDLD may be explained in part by an altered membrane permeability of the superficial epithelial cells. An association with developmental delay has not been reported previously.

Clinical and ultrastructural findings in mare's tail lines of the corneal epithelium.

AIMS: Mare's tail lines are uncommon, grey, parallel, tapering epithelial lines, which may give rise to discomfort or to visual symptoms. The authors report the clinical and ultrastructural findings in two patients METHODS: Therapeutic debridement was performed in two patients suffering from mare's tail disorder. The loosely attached epithelium was removed and fixed in glutaraldehyde containing cuprolinic blue and processed in a standard fashion for electron microscopy. RESULTS: Ultrastructural studies showed an avascular, collagenous pannus extending under the whole of the excised epithelium in each case and separated from it by a thickened basal lamina like zone. The basal laminar material extended into the epithelium in folds, in keeping with the clinical features. Interesting ultrastructural features included: (1) a lack of hemidesmosomes in relation to the basal laminar material; (2) trapping of degenerate keratocytes within the invaginating basal laminar folds; (3) an unusual regularity and fine dimensions of the collagen fibrils and proteoglycans making up the subepithelial pannus. The basal laminar material contained proteoglycans and small fibres similar in appearance to long spacing collagen. CONCLUSIONS: Mare's tail lines are caused by basal laminar material, assumed to be chiefly of epithelial origin, which invaginates the corneal epithelium. The presence of occasional keratocytes within the invaginating folds suggests that there may be a stromal contribution to the disorder. The visibility of mare's tail lines in the focal beam of the slit lamp is likely to be related to the thickness and light scattering properties of the invaginations and of the subepithelial deposits. Tractional forces, imposed by lid action, could explain their horizontal disposition.

Functional aspects of the tear film lipid layer.

The lipid layer is an essential component of the tear film, providing a smooth optical surface for the cornea and retarding evaporation from the eye. The meibomian lipids which compose it are well adapted for this purpose. They form a thin, smooth film whose thickness, and probably composition, influences the rate of evaporation. Their melting range ensures sufficient fluidity for delivery to the tear film from the lid margin reservoirs, while the film itself may exhibit a higher viscosity at the cooler temperature of the ocular surface. The factors governing lipid film formation during the blink are not fully understood, but one view is that the polar lipids, interacting with the aqueous sub-phase of the tear film, spread in advance of the non-polar components, which form the bulk of the film. The meibomian lipids stabilise the tear film by lowering its free energy; they carry water into the film during its formation and interact with lipid-binding proteins in the aqueous phase, such as tear lipocalin. The lipocalins, complexed with other tear components, may also contribute to the high, non-Newtonian viscosity of the tear film and its low surface tension, features which are essential for tear film stability. Formation of the lipid film is a complex process. Lipid is delivered to the tear film in the up-phase of the blink, more from the lower than the upper reservoir. The lipid layer comes to a stop well after completion of the blink and remains relatively immobile until it is compressed in the down-phase of the blink that follows. Then, it either retains its structure in a series of subsequent blinks, or is completely re-constituted after mixing with the reservoir lipids. Delivery of meibomian lipid to the marginal reservoirs is mainly the result of continuous secretion, under neural and hormonal control, supplemented by lid action. The reservoirs provide a hydrophobic barrier to tear overspill and to contamination by skin lipids which might destabilise the tear film. They probably also provide the chief route for meibomian lipid excretion.

The contribution of meibomian disease to dry eye.

The tear film lipid layer is the major barrier to evaporation from the ocular surface. A decrease in its thickness or functional integrity may cause evaporative dry eye (EDE). Obstructive meibomian gland dysfunction (MGD) is the most common cause of EDE and occurs as a primary disorder or secondary to acne rosacea, seborrheic or atopic dermatitis, and with cicatrizing conjunctival disorders, such as trachoma, erythema multiforme, and cicatricial pemphigoid. MGD may be an incidental finding in asymptomatic eyes, or it may be responsible for irritative lid symptoms in the absence of dry eye. MGD-dependent EDE is diagnosed on the basis of a defined degree of MGD in a symptomatic patient showing typical ocular surface damage in the absence of an aqueous tear deficiency. When MGD occurs in a background of aqueous tear deficiency (ATD), then an additional evaporative component may assumed, depending on the extent of meibomian obstruction. However, definitive criteria are not yet established. The clinical severity of dry eye is greatest when ATD and EDE occur together, particularly in Sjogren syndrome. A hypothesis is proposed to explain the steps leading to primary, simple MGD and subsequent EDE.

Differential effects of aging on transport properties of anterior and posterior human sclera.

The transport properties and composition of 44 pairs of human sclera, 37-91 years were compared. Solute transport, diffusion and partition coefficients of posterior sclera for solutes ranging in mass from 0.023-70kDa were higher than those of anterior sclera; the posterior region was also more hydrated. The differences in partition coefficient between anterior and posterior sclera became more pronounced as solute molecular weight increased. Partition coefficients and hydration of both regions decreased with increasing age. Chondroitinase ABC digestion, which removed the majority of glycosaminoglycans, increased partition coefficients of both regions significantly. These results suggest that for regions of equal scleral thickness, neglecting the influence of vascular factors, drug delivery will be more readily achieved across the posterior sclera than the anterior sclera in the age group studied and that, for both regions, ease of delivery will decrease with decreasing age.

Diagnosis of dry eye.

Dry eve disease is characterized by symptoms, ocular surface damage, reduced tear film stability, and tear hyperosmolarity. There are also inflammatory components. These features can be identified by various kinds of diagnostic tests (symptom questionnaires, ocular surface staining, tear break-up time, and osmometry), although there may not be a direct correlation between the number or severity of symptoms and the degree of ocular surface damage or tear deficiency. Once the diagnosis of dry eye disease has been established, further tests can be used to classify the condition into tear-deficient or evaporative dry eve. The two forms of dry eye are not mutually exclusive and often co-exist. The optimal diagnosis of dry eye disease, therefore, depends on the results of several tests, and this article suggests an appropriate order for performing these tests at a single clinic visit.

Intraocular vancomycin levels after intravitreal injection in post cataract extraction endophthalmitis.

PURPOSE: Intravitreal antibiotics are the mainstay of treatment of endophthalmitis following cataract surgery. The purpose of this study is to determine the range of intraocular vancomycin found after intravitreal therapy and assess the optimum time for repeat injections. METHODS: Aqueous and vitreous vancomycin was assayed at the time of reinjection in 14 patients with endophthalmitis showing a poor clinical response after their primary injection. Nine patients received vancomycin 2 mg and another five received vancomycin 1 mg. In six patients the injection was repeated at 48 hours and in seven at 72 hours. Two patients received three injections. RESULTS: Aqueous vancomycin varied from 8.4 to 170 mg/L and the vitreous vancomycin level ranged from 21.2 to 220 mg/L. CONCLUSIONS: In the current study vitreous vancomycin levels were variable, but well within the therapeutic range for sensitive Gram-positive organisms. At times they exceeded the putative retinotoxic levels (100 mg/L). Higher aqueous levels were found after an injection of 2 mg than after 1 mg. Vancomycin levels were still very high 3 days after injection of 2 mg where results were available. Assay at the time of repeat injection may provide insight into the adequacy of vitreous levels and guide future therapy.

Congenital hereditary endothelial dystrophy and band keratopathy in an infant with corpus callosum agenesis.

PURPOSE: To report the features of a syndrome of endothelial failure and band-shaped keratopathy in an infant with corpus callosum agenesis. METHODS: The clinical and histopathologic features of an infant presenting with bilateral corneal clouding and corpus callosum agenesis are reported. The patient underwent bilateral penetrating keratoplasty at ages 28 months and 4 years. Light and electron microscopy were used to characterize the structural changes. RESULTS: The epithelium was thin and degenerate. Bowman's membrane contained spherical aggregates that were present also within a connective tissue pannus. The midstroma was normal, but there were floral and rope-like aggregations of collagen in the pre-Descemet's membrane region. Under electron microscopy, the spherules formed target-shaped lesions with a central focus of alternating electron-dense and lucent material. Numerous microfilaments in the pannus and anterior stroma labeled with fibrillin-1 antibody. Microfilaments within fibroblasts were stained with vimentin antibody. Posteriorly, the endothelium was mainly absent and Descemet's membrane showed a fetal layer and a posterior collagenous layer. CONCLUSION: Corneal appearances in this patient were in keeping with those of congenital hereditary endothelial corneal dystrophy. However, there was no family history and neither parent showed a clinical endothelial abnormality. The presence of fetal, banded material in Descemet's membrane suggested that endothelial loss began at or near the time of birth. The band keratopathy was regarded as a secondary change. The association with corpus callosum agenesis does not appear to have been described previously.

Ultrastructural morphology and expression of proteoglycans, betaig-h3, tenascin-C, fibrillin-1, and fibronectin in bullous keratopathy.

AIMS: To investigate the ultrastructural localisation of proteoglycans (PG), betaig-h3 (keratoepithelin), tenascin-C (TN-C)), fibrillin, and fibronectin in bullous keratopathy (BK) corneas. METHODS: Five corneas from cases of pseudophakic bullous keratopathy (BK) were examined by electron microscopy. PG were demonstrated using cuprolinic blue, and the proteins betaig-h3, TN-C, fibrillin, and fibronectin were immunolocalised with rabbit anti-betaig-h3, mouse anti-TN-C (BC10 and TN2), mouse anti-fibrillin-1 (MAB2502), mouse anti-fibrillin (MAB1919), and rabbit anti-fibronectin by using a standard immunogold technique. RESULTS: Epithelial cells contained numerous vacuoles. Epithelial folds and large, electron lucent subepithelial bullae were present. Basal lamina was thickened and traversed by disrupted anchoring filaments. In the stroma, interfibrillar collagen spacing was increased and abnormally large PG were present. Descemet's membrane (DM) contained lucent spaces in which there were small filaments. Keratocyte and endothelial cells contained melanin granules. A posterior collagenous layer (PCL) contained numerous microfilaments and wide spacing collagen fibres with a periodicity of 100 nm. Large quantities of abnormal PG were observed at the endothelial face of the PCL. Very strong labelling with betaig-h3 antibody was observed in the basement membrane, Bowman's layer, stroma, DM, and PCL, but not in keratocytes and endothelial cells. Strong labelling with BC10 and TN2 was seen below the epithelium, in electron lucent spaces where the hemidesmosomes were absent, in the fibrotic pannus, in parts of Bowman's layer, the stroma, and Descemet's membrane. Labelling with BC10 was stronger and more evenly distributed than with TN2. Fibrillin-1 (MAB2502) and fibrillin (MAB1919) labelling was similar to TN-C labelling. Fibrillin (MAB1919) labelling was stronger than fibrillin-1 (MAB2502) labelling. CONCLUSIONS: Immunoelectron microscopy showed precise labelling of proteins at both the cellular and the subcellular level. Expression of proteins betaig-h3, TN-C, fibrillin, and fibronectin was highly increased compared with normal cornea. In the oedematous stroma, increased collagen fibril separation may facilitate a wider distribution of some soluble proteins, such as betaig-h3, throughout stroma. The modified expression of the proteins studied in these cases of BK may be regarded as part of an injury response.

Posterior subcapsular and nuclear cataract after vitrectomy.

PURPOSE: To examine the morphological changes in the postvitrectomy lens and to monitor the development of these changes over time. SETTING: Oxford Eye Hospital, Oxford, United Kingdom. METHODS: In this prospective study, 33 consecutive phakic patients having pars plana vitrectomy were recruited. Cataract development was quantified by clinical grading and digital Scheimpflug image analysis. Slitlamp biomicroscopy and photography were used to document the morphological appearance. The main outcome measures were the incidence, morphology, and development of posterior subcapsular and nuclear cataract. RESULTS: A characteristic, transient posterior subcapsular cataract (PSC) was present in 89% (17 of 19) of tamponade patients within 24 hours of surgery. Of the patients who had vitrectomy without tamponade, 9% (1 of 11) developed similar changes. Nuclear opacity developed in 61% (11 of 18) of tamponade patients and in 50% (3 of 6) of nontamponade patients. A longer term retrospective review of the same patients' case notes revealed nuclear cataract in 67% (12 of 18) of tamponade cases and 30% (3 of 10) of nontamponade cases. Eighteen percent (2 of 11) of nontamponade cases and 67% (14 of 21) of tamponade cases had cataract surgery after a 10.7 month and a 12.4 month follow-up, respectively. CONCLUSIONS: Vitrectomy and tamponade produced a characteristic transient PSC in the immediate postoperative period. Disruption of fluid balance in the region of the posterior lens was suggested by the morphological appearance. The acute changes resolved but were followed by accelerated nuclear opacification.