| Objective: to search the clinic features, nosogenesis and treating methods ofHepatic cortical blindness. Method: to analyse the causes, clinic features,treating，outcomes of12patiences with Hepatic cortical blindness the law inthe changes of electrolytes in blood serums in the patients with Hepatic CorticalBlindness；to test the significances of the centralization tendency and thedisperse tendency of the K+,Na+and Cl-in the blood serums by three groups ofpeople, among which are12patients with Hepatic cortical Blindness(hereinafter HCB group),12patients with hepatic encephalopathy (hereinafterHE group) and12healthy people (hereinafter Healthy group). Output: Allcases are developed from severe hepatitis or liver cirrhosis, with a morbidity rateof2.05%. The incentives of the disease include fatigue, gastrointestinal blooding,high protein diet, electrolyte imbalance, etc. The clinic features includetemporary blindness, possibly associating with conscious disturbance in variousdegrees. They may also include no-response by twinkling of eyes under stronglight irradiation or external terrifying stimulation, equal sizes of opposite pupils,exsitence of light reaction; there is no organic disease in fundus, visual paths orintracalvarium. Active treatment of the hepatic encephalopathy improves thehealth by100%. Measured against the Healthy group, the HCB group and theHE group have lower contents of K+and Na+in the blood serums with p<0.05;The coefficient of variation of Potassium in the HCB group is larger than that ofthe HE group with p<0.05. Conclusion: Hepatic cortical blindness has a lowmorbidity rate. It is rare in clinic, easy to be missed or misdiagnosed. Oncehappens, it could be regarded as a special symptom of hepatic encephalopathy;the parameters and changes of K+and Na+in the blood serums of HCB and HEcases are significantly different from those of the healthy people; the K+in theblood serums of the HCB cases have a larger degree of variation than that of theHE cases. |
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