الفهرس 
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Abstract
Hepatorenal syndrome is a clinical condition that occurs in patients with chronic liver disease, advanced liver cell failure and portal hypertension characterized by impaired renal function and marked abnormalities in the arterial circulation and activity of the endogenous vasoactive system&Frerichi and Flint made the original description of renal function disturbances in liver disease (Arroyo et al., 2013).
They describe the development of oliguria in patients with chronic liver disease in the absence of proteinuria and normal renal histology, they proposed, that abnormality in renal function was related to disturbances present in the systemic circulation(Arroyo et al., 2013).
Renal failure in hepatorenal syndrome was due to extensive vasoconstriction of renal circulation and paved the way to large number of studies assessing the role of vasoactive substances in the pathogenesis of renal hypoperfusion in hepatorenal syndrome (Epstein et al., 2014).People of all races and who have chronic liver disease are at a risk for hepatorenal syndrome (Betrosianet al., 2007).
Type I HRS occurs in approximately 25% of patients with SBP, despite rapid resolution of the infection with antibiotics(Betrosian et al., 2007). Without treatment, the median survival rate with type 1 hepatorenal syndrome is less than 2 weeks and virtually all patients die within 10 weeks after the onset of renal failure(Salerno et al., 2007).
The aims of our study is to assess outcome of hepatorenal syndrome in Sohag University Hospitals and discover possible predictors of non-survival.
The study included 50 patient attented Sohag University hospital who were studied prospectively to observe clinical outcome and Various variables were studied between survivor and non-survivor groups in hepatorenal syndrome .
Statestics showed that:
The mean age of the study group was (65+-13 years ) the mean age of survivors group was 60 year and its range was (40-87), while the mean age for non-survivors group was 66 year and its range was (39-91).
36 patients were males (72%) and 14 patients were females (28%), percentage of males to females was equal in survivor group (50%: 50%),
19 patients were diagnosed as SBP (38%), 2 patients only had SBP in the survivor group (14.29%), esophageal varices present in(40%) of the pateints, 5 patients had varices in the survivor group (35.71%), while 15 patients had varices in the non-survivor group (41.67%).
As regard the child score, majority of the patients in the survivor group were child B (12 patients,( 85.71%) while in the non-survivor group the majority were child C (33 patients, 91.67%).
Half of patients of the study group were type I and 50% the others were type II,the majority of the patients in the survivor group were type II hepatorenal syndrome (12 patients, 85.71%),
Renal impairement in the non-survivor group was higher than in the survivor group as the mean of creatinine in the survivor group was 3.7 (SD: 1.26; range: 2-6) and was 5.94 in the non-survivor group (SD: 3.07; range: 2.715).
Coagulopathy was present in more than 90% of the patients and patients in the non-survival group had significant coagulopathy as compared to survivors.
Dialysis was done to only 7 participants (14%) , none of the patients of the survivor group received dialysis, while dialysis was done to 7 patients from the non-survivor group (19.44%).
Regarding manegment with terillipressin 17 patients from our study group received terillipressin (34%), while, the remaining participants (33, 66%) did not received.
Conclusion:
the study showed that HRS is aserious complication of advanced liver cirrhosis with high mortality rate, 14 patients (28%) were survivors, but the remaining 36 patients were non-survivors (72%).
And showed that the possible predicting factors of mortality included male sex,having tense ascites, having SBP,hepatic encephalopathy being child score C, type I HRS,with high level of serum creatinine and urea,low level of serum albumin. These factors were be subjected to multivariate regression analysis.
RECOMMENDATIONS
1-Decompensated cirrhotic patient must be routinely investigated for renal impairment to avoid rapid deterioration and to insure proper management at time and transfer to liver transplant unit if needed.
2- Rapid diagnosis of the cause of renal impairment in decompensated cirrhotic patient to treat correctable cause.
3-Rapid detection and treatment of SBP to inhibit deterioration of kidney function.
4-Infections other than SBP should be promptly identified and vigorously treated to minimize the risk of HRS,debilitated patients with advanced cirrhosis often have chronic leukopenia and may not develop leukocytosis or fever, even with severe infections, a high index of suspicion is necessary to identify infections early in decompensated cirrhotics
5-optimal management of refractory ascites or severe hyponatremia could reduce the risk of developing type 2 HRS.