Ruthenium-106 plaque brachytherapy for symptomatic vasoproliferative tumours of the retina.

AIM: To investigate the safety and efficacy of beta ray brachytherapy in treatment of vasoproliferative tumours of the retina (VTR). METHODS: 35 consecutive patients with symptomatic VTR were treated with a ruthenium-106 ((106)Ru) plaque. Three tumours had been treated previously (two with cryotherapy; one with transpupillary thermotherapy). 32 VTR (91.4%) were located in the lower half of the retina and all of them were found between the mid-periphery and the ora serrata. The mean tumour thickness was 2.8 mm. An exudative retinal detachment was present in 25 eyes (71.4%) and in 15 cases (42.9%) hard exudates were found in the macula. The major symptom was loss of vision (77.1%). RESULTS: Brachytherapy was well tolerated by every patient. The mean applied dose was 416 Gy at the sclera and 108 Gy at the tumour apex. In all but four eyes (88.6%), it was possible to control the VTR activity. The median follow up time was 24 months. Three of the above mentioned four eyes with treatment failure had had secondary glaucoma before therapy. There was no case of radiation induced neuropathy or retinopathy. Cataract surgery was necessary for five patients. The development of epiretinal gliosis was the most common event during follow up (n = 10, 28.6%). The mean visual acuity decreased slightly (0.33 before and 0.29 after brachytherapy). Multivariate analysis showed that the presence of macular pathology before treatment was associated with a 6.1-fold risk of vision of 0.25 or better (p = 0.03). CONCLUSIONS: beta ray brachytherapy with (1106)Ru plaques was able to control the activity of VTR and retain vision. Cases with secondary glaucoma before treatment had a very poor prognosis.

Vasoproliferative tumours of the retina.

BACKGROUND: Vasoproliferative tumours of the retina (VPTR) are benign tumours of unknown origin, occurring mostly in otherwise healthy patients. VPTR may be associated with other chorioretinal diseases, such as uveitis. The tumours, which histologically represent reactive gliovascular proliferations, are characterised by a pink to yellow appearance on funduscopy and are accompanied by exudative and haemorrhagic changes of the retina. METHODS: 22 cases of VPTR in 21 patients were examined with a follow up period between 1 month and 6 years. Ophthalmological changes associated with VPTR were intraretinal and subretinal exudations (n=18), exudative detachments of the surrounding sensory retina (n=13), intraretinal and subretinal haemorrhages (n=10), exudative changes within the macula (n=10), hyperpigmentation of the retinal pigment epithelium at the border of the exudative retinal changes (n=9), and vitreous haemorrhages (n=4). Tumour biopsy was performed in two cases. Treatment consisted of plaque radiotherapy (n=14), plaque radiotherapy and cryotherapy (two), cryotherapy only (two), observation (three), and enucleation in one case of a blind and painful eye. RESULTS: Regression of the tumour and the associated exudative changes could be observed in all treated cases. Visual acuity at last follow up improved two lines or more in two cases, remained within two lines of the initial visual acuity in 15 cases, and worsened in the remaining five. Histopathological examination of the biopsy specimens and the tumour of the enucleated eye showed massive capillary proliferation with perivascular spindle-shaped glial cells of retinal origin. CONCLUSION: The correct diagnosis of VPTR is of importance as these lesions may lead to visual loss. Further, VPTR must be differentiated from angiomas associated with von Hippel-Lindau disease as well as from ocular and systemic malignancies. Regression of tumour thickness and associated retinal changes can be achieved with brachytherapy or cryotherapy.

Value of transesophageal echocardiography, esophago-gastroduodenoscopy and retinoscopy prior to intra-arterial fibrinolytic therapy in patients with peripheral arterial disease.

BACKGROUND: We prospectively investigated the need for esophagogastroduodenoscopy (EGD), transesophageal echocardiography (TEE) and retinoscopy for pre-interventional screening in patients with peripheral arterial occlusive disease (PAD) prior to intraarterial fibrinolytic therapy. PATIENTS AND METHODS: 212 consecutive patients suffering from PAD (164 male and 48 female, mean age: 64 +/- 11 years, 161 patients stage II of Fontaine's classification, 10 patients at stage III and 41 patients at stage IV) referred for interventional treatment were included. 173 EGDs, 169 TEEs and 188 retinoscopies were performed within one week prior to fibrinolysis. 114 patients had all three examinations. RESULTS: Pathologic findings were detected in 56 (49%) of the 114 patients: 23 erosions, 12 ulcers, 2 esophagites, 1 gastric carcinomata, 3 intracardiac thrombi, 5 aortic thrombi, 11 diabetic and 5 hypertensive retinopathies and 1 with retinal aneurysms. 30 patients (25%) received fibrinolytic therapy, despite a contraindication: The one patient with ventricular thrombus was treated as an ultimate therapy, and amputation was prevented. Two patients showing plaques covered by large thrombi in the descending thoracic aorta were treated because cranial embolism should not occur. Four diabetic patients with multilevel disease, severe claudication and prior retinal bleeding were treated. Fibrinolytic therapy was started on 23 patients after complete healing of the mucosal lesions. CONCLUSION: TEE revealed potential sources of embolization in 4% of the patients and is justified to reduce the individual risk. Retinoscopy should be done in patients with diabetes mellitus and hypertension, and if prior bleeding is present fibrinolysis should be done only if other treatment-regimes are not available.