Objective To observe the clinical effect of intravenous thrombolytic therapy for central retinal artery occlusion (CRAO) with poor effect after the treatment of arterial thrombolytic therapy. Methods Twenty-four CRAO patients (24 eyes) with poor effect after the treatment of arterial thrombolytic therapy were enrolled in this study. There were 11 males and 13 females. The age was ranged from 35 to 80 years, with the mean age of (56.7±15.6) years. There were 11 right eyes and 13 left eyes. The visual acuity was tested by standard visual acuity chart. The arm-retinal circulation time (A-Rct) and the filling time of retinal artery and its branches (FT) were detected by fluorescein fundus angiography (FFA). The visual acuity was ranged from light sensation to 0.5, with the average of 0.04±0.012. The A-Rct was ranged from 18.0 s to 35.0 s, with the mean of (29.7±5.8) s. The FT was ranged from 4.0 s to 16.0 s, with the mean of (12.9±2.3) s. All patients were treated with urokinase intravenous thrombolytic therapy. The dosage of urokinase was 3000 U/kg, 2 times/d, adding 250 ml of 0.9% sodium chloride intravenous drip, 2 times between 8 - 10 h, and continuous treatment of FFA after 5 days. Comparative analysis was performed on the visual acuity of the patients before and after treatment, and the changes of A-Rct and FT. Results After intravenous thrombolytic therapy, the A-Rct was ranged from 16.0 s to 34.0 s, with the mean of (22.4±5.5) s. Among 24 eyes, the A-Rct was 27.0 - 34.0 s in 4 eyes (16.67%), 18.0 - 26.0 s in 11 eyes (45.83%); 16.0 - 17.0 s in 9 eyes (37.50%). The FT was ranged from 2.4 s to 16.0 s, with the mean of (7.4±2.6) s. Compared with before intravenous thrombolytic therapy, the A-Rct was shortened by 7.3 s and the FT was shortened by 5.5 s with the significant differences (χ2=24.6, 24.9; P＜0.01). After intravenous thrombolytic therapy, the visual acuity was ranged from light sensation to 0.6, with the average of 0.08±0.011. There were 1 eye with vision of light perception (4.17%), 8 eyes with hand movement/20 cm (33.33%), 11 eyes with 0.02 - 0.05 (45.83%), 2 eyes with 0.1 - 0.2 (8.33%), 1 eye with 0.5 (4.17%) and 1 eye with 0.6 (4.17%). The visual acuity was improved in 19 eyes (79.17%). The difference of visual acuity before and after intravenous thrombolytic therapy was significant (χ2=7.99, P＜0.05). There was no local and systemic adverse effects during and after treatment. Conclusion Intravenous thrombolytic therapy for CRAO with poor effect after the treatment of arterial thrombolytic therapy can further improve the circulation of retinal artery and visual acuity.
In order to summarize the experience in the treatment of ischemic necrosis of lower extremities resulted from thrombotic occluded angittis, 15 cases were reported, which were treated by primary arterization in situ of V. Saphena magna. With a period of follow-up, 4-26 months on the average, it was found that symptoms in 14 cases were much allayed obviously, except 1 case with little relief. It suggested that primary arterization in situ of V. saphena magna could improve the circulation of the ischemic extremity rapidly without any influence of venous reflux.
Objective To observe the change of diffusion upper limit of macromol ecules through pathological retina and the difference between the layers of retina. Methods Retinal edema was emulated by establishing branch retinal vein occlusion (RVO) model in miniature pig eyes under photodynamic method. Two days later, the retinas of both eyeballs were peeled off. The diffusion test apparatus was designed by ourselves. FITC-dextrans of various molecular weights (4.4, 9.3, 19.6, 38.9, 71.2 and 150 kDa) and Carboxyfluorescein (376 Da) were dissolved in RPMI1640 solutions and diffused through inner or outer surface of retina. The rate of transretinal diffusion was determined with a spectrophotometer. Theoretical maximum size of molecule (MSM) was calculated by extrapolating the trend-linear relationship with the diffusion rate. In separate experiments to determine the sites of barrier to diffusion, FITC-dextrans were applied to either the inner or outer retinal surface, processed as frozen sections, and viewed with a fluores cence microscope. Results FITC-dextrans applying to inner retinal surface, 4.4 kDa dextrans were largely blocked by inner nuclear layer (INL); 19.6,71.2 kDa dextrans were blocked by the nerve fiber layer (NFL) and inner plexiform layer; 15.0 kDa dextrans were blocked by NFL. FITC-dextrans applying to outer retinal surface, most dextrans with various molecular weights were blocked before outer nuclear layer (ONL). No matter applying to the inner or outer surface, Carboxyfluore scein can diffuse through the whole retina and aggregate at INL and ONL. After RVO, the inner part of retina became edema and cystoid, loosing the barrier function. Compared with the normal retina, the MSM in RVO tissues increased (6.5plusmn;0 39nm Vs 6.18plusmn;0.54nm, t=4.143, P=0.0001). Conclusions A fter RVO, the barrier function of inner part of retinal is destroyed and the upper limit of diffusion macromolecule size increased, which is nevertheless limited. ONL acts as bottle-neck barriers to diffusion, if the outer part of retina is damaged, the change of the diffusion upper limit will be prominent. （Chin J Ocul Fundus Dis，2008，24：197-201）