[Bacterial infection and its relation to the genesis and course of varicose hemorrhage].

Acute hemorrhage from esophageal varices due to portal hypertension is a frequent and serious complication of liver cirrhosis. Bacterial infection may be one of the factors influencing such hemorrhage. Endotoxins may increase portal tension and at the same time result in primary hemostasis disorder, thus becoming one of the causes of hemorrhage. The authors of the paper compared the incidence of bacterial infection in 53 patients with varicose hemorrhage due to portal hypertension with 62 patients with liver cirrhosis and portal hypertension without varicose hemorrhage. At least one pathogen was found in considerable 61.1% of the total of patients in the liver cirrhosis group, while the difference between the two groups was but insignificant. No statistically significant difference was found between the group of patients with hemorrhage and those without hemorrhage in terms of presence of bacterial infection in hemoculture, urine, throat, faeces and ascites, nor was there a difference in the etiology of the G+ bacteria, G- bacteria or fungi and yeast infectious agents in the hemoculture, urine, throat, faeces and ascites in either of the groups. No statistically significant difference was found in comparing the patients with a recurrence of hemorrhage (or with mortality) and with infection with those without recurrence of hemorrhage. Bacterial infection was more often found in patients with a recurrence of hemorrhage (75%) as compared with those without any recurrence (52%), and also in patients who died bacterial infection was proven more often than in those who survived (61.9% vs. 58.1%, respectively). There was no difference in morbidity or recurrence of hemorrhage between the patients treated with norfloxacin and ampicilin/sulbactam. No statistically significant difference was recorded between the 1st and 5th day in terms of decrease in bacterial infection. A significant difference was found in the urine etiological agent, where a significant increase in the share of fungal and yeast urine infection (p = 0.011) was recorded after the application of the therapy, as well as a drop in urine infection caused by the G- bacterial agent (p = 0.057).