Central corneal thickness in osteogenesis imperfecta and otosclerosis.

The central corneal thickness was measured in 53 patients with osteogenesis imperfecta. The average thickness was found to be 0.443 +/- 0.003 (SEM) mm. This value was significantly lower than the central corneal thickness in 35 patients with otosclerosis (0.515 +/- 0.004 mm) and in 35 sex- and age-matched normal control subjects (0.522 +/- 0.004 mm). No difference in corneal thickness between otosclerosis and controls was observed. Measurements of the central corneal thickness may be of great value in the diagnosis of osteogenesis imperfecta.

Central corneal thickness and intraocular tension in patients with acromegaly.

In 27 patients with pituitary adenomas the central corneal thickness and the intraocular tension were measured. Thirteen of the patients were suffering from acromegaly, and in this group the central corneal thickness was 0.561 mm +/- 0.35 (mean +/- SD). In the 14 patients with pituitary adenomas but no acromegaly the central corneal thickness was 0.526 mm +/- 0.030 (mean +/- SD). This difference is statistically significant 0.01 greater than P greater than 0.001. In the 13 patients with acromegaly the intraocular tension measured by applanation was 16.9 mmHg +/- 2.3 (mean +/- SD) and in the control group 14.7 mmHg +/- 2.4 (mean +/- SD). This difference is statistically significant (0.05 greater than P greater than 0.02). When the applanation reading is corrected for the difference in the central corneal thickness, the patients suffering from acromegaly have an intraocular tension of 14.1 mmHg, which is of the same magnitude as the tension in the patients without acromegaly.

Influence of tranexamic acid and acetylsalicylic acid on the thickness of the normal cornea.

In a masked cross-over study ten normal subjects were treated with tranexamic acid and acetylsalicylic acid one g three times daily for seven days. The central corneal thickness. was found to increase in response to acetylsalicylic acid and to decrease in response to tranexamic acid. This finding provides evidence for the involvement of the fibrinolytic system in the regulation of the normal corneal thickness. The endothelial morphology, as seen with the specular microscope, was unchanged during treatment with either drug.

Fibrinolytic factors in aqueous humour and serum from patients with Fuchs' dystrophy and patients with cataract.

The concentration of alpha 2-macroglobulin, alpha 1-antitrypsin, plasminogen, C3-complement, fibrinogen degradation products (FDP) and fibrinolytic activity, were studied in the aqueous humour and serum from nine patients with Fuchs' endothelial dystrophy, 17 patients with uncomplicated senile cataract and in the secondary aqueous from six cataract patients. Finally, the aqueous humour and serum from two patients anterior uveitis were studied. An increased concentration of alpha 2-macroglobulin, alpha 1-antitrypsin, plasminogen and C3-complement was found in both the aqueous and the serum from patients with Fuchs' dystrophy when compared with the primary aqueous and serum from patients with cataract but this was only significant for alpha 1-antitrypsin in aqueous humour. A significant increase in the amount of FDP was found in the serum of the Fuchs' patients compared with the cataract patients. Fibrinolytic activity could not be demonstrated in the serum in any of the patient groups. The concentrations of the various factors found in the secondary aqueous of the cataract patients differed only slightly from the content of the primary aqueous of the Fuchs' patients.

Fibrinolysis and traumatic hyphaema.

Since January 1st 1975, 310 patients with traumatic hyphaema have been treated with the antifibrinolytic drug tranexamic acid. One secondary haemorrhage has occurred, corresponding to a frequency of secondary haemorrhage of 0.32%. Eighty-five of these patients were treated as out-patients. In four patients with traumatic hyphaema, who were not treated with tranexamic acid, the serum content of activator inhibitor was determined daily. An increase was seen during the first five days after the trauma, followed by a marked fall on the 6th day. In the same four patients, the central corneal thickness was followed by daily measurements and compared to the variation in activator inhibitor.

Serum and aqueous humour concentration of tranexamic acid after peroral administration.

After a single oral dose of 25 mg/kg tranexamic acid in 37 patients with cataract as the sole eye disease, the concentration of the drug was measured in both the serum and the aqueous at various intervals following intake. The serum concentration was highest after three h (average 15.44 mg/l), but a trace of tranexamic acid (0.7 mg/l) could still be found after 19 h. In the aqueous, the concentration was likewise highest after three h (average 1.62 mg/l), but, following this, the fall in tranexamic acid concentration was very gradual and after 19 h was found to be 1.3 mg/l. In two patients who had received 25 mg/kg three times daily for three days, an aqueous concentration of 2.3 mg/l was found eight h after the final intake.

Early postoperative changes in graft thickness after penetrating keratoplasty. Influence of host corneal disorder on time course.

In 172 patients the thickness of the corneal graft was followed with frequent measurements during the first 14 days after operation. Three different graft thickness time courses were observed. Patients with keratitis, stromal dystrophy and corrosion or mechanical lesion showed a secondary rise in graft thickness on the 6th postoperative day, while patients with keratoconus and those treated with tranexamic acid showed no rise on the 6th day. Patients with Fuchs' dystrophy differed from the other groups in not reaching the maximal thickness until the 3rd postoperative day. The possible correlation of these three time courses with changes in the fibrinolytic system is discussed.

The effect of urokinase on central corneal thickness and vitreous haemorrhage.

Thirteen patients with vitreous opacities were treated by intravitreal injection of urokinase. The central corneal thickness was measured daily on both eyes. Determination of visual acuity and ophthalmoscopy were done before treatment and at each following attendance (longest period of follow-up was seven months). The central corneal thickness increased after urokinase injection and the maximum thickness was reached on the second day. On the 6th day a secondary rise in corneal thickness occurred. The possible relation to the fibrinolytic system is discussed. There was an effect on the vitreous opacities in 8 out of 13 eyes. Only in 3 of the 13 eyes did visual acuity increase. This relative poor result as regards visual acuity in most cases was due to membranes in the vitreous.

Management of late corneal graft problems.

Immediately after an operation the corneal graft is taken care of by the surgeon, but after a certain period of time the control lies in the hands of the general ophthalmologist. Examples of the management of different kinds of postoperative complications are presented. Early correct treatment of any graft problem is of decisive importance. Careful slit-lamp examination and measurement of graft thickness is stressed and the prompt use of systemic and subconjunctival steroids is recommended for incipient graft failure. Systemic tranexamic acid may also be useful.

A double-blind study on the influence of tranexamic acid on the intraocular pressure and the central corneal thickness after trabeculectomy for glaucoma simplex.

The influence of tranexamic acid on the intraocular pressure and central corneal thickness has been examined by means of a double-blind trial in patients with glaucoma simplex. The material comprised 28 patients (14 pairs) who had all been operated on for glaucoma in one eye by trabeculectomy. Tranexamic acid was found not to influence the intraocular pressure, neither in the operated eye nor in the opposite eye. The possible antifibrinolytic effect on the outflow of the aqueous humour is discussed. As in previous studies an effect of tranexamic acid on the central corneal thickness was found in both the operated and in the non-operated eye. A possible mechanism behind this is discussed.

Central thickness in corneal disorders.

In the single individual the central corneal thickness (CCT) shows only small variations. Therefore CCT has been studied in a number of corneal diseases in order to investigate if this dimension might contribute to the diagnosis or to the understanding of the pathogenesis. Normal CCT was found in hereditary dystrophies with the exception of the macular dystrophy of Groenouw (type II), which showed a significantly reduced thickness. Reduced CCT was found in chronic degenerations of leutic, tuberculous or indefinite nature. Marginal degenerations of Fuchs-Terrien type also showed reduced CCT. The possible role of abiotrophic processes in this corneal thinning is dicussed. Endothelial dysfunction is indicated by increased CCT. This occurs in bullous keratopathy and in many acute disorders. Vascularisation of the cornea does not preclude the occurrence of normal or even reduced thickness.

Effect of tranexamic acid on choroidal melanoma.

Four cases of malignant choroidal melanoma have been treated with the antifibrinolytic agent tranexamic acid (Cyklocapron). One patient treated for six months showed no progression in tumor growth. Three eyes have been enucleated, and the histological examination revealed that the tumours were surrounded by fibrin. No side-effects of the treatment were observed.

A double-blind study of the influence of tranexamic acid on the central corneal thickness after cataract extraction.

A double-blind study of the influence of systemic tranexamic acid on the central corneal thickness after cataract extraction was performed in 17 pairs of patients. Apart from the cataract, no were present. A sequential statistics was used to show that the increase in central corneal thickness after operation was significantly less in the tranexamic acid treated group than in the placebo group. There was no significant difference in intraocular pressure between the tranexamic acid and the placebo treated group. The possible influence of tranexamic acid on the thickness controlling mechanism of the cornea is discussed, and studies concerning the fibrinolytic system, the complement system and the aqueous humour amino acid treated patients are mentioned.