You are on page 1of 30

Diambil dari :Juan Cordoba et al. Journal of Hepatology 2014 vol.

60 j 275–281

Pembimbing Dipresentasikan

: dr. Putut Bayu Purnama, Sp. PD KGEH : dr. Meldy Muzada Elfa

Latar belakang
Hepatic encephalopathy (HE) is a common complication of cirrhosis [1,2] Recently, acute-on-chronic liver failure (ACLF) was defined by the Canonic Study 1. acute decompensation of cirrhosis (ascites, HE, gastrointestinal hemorrhage, bacterial infections or any combination of these) 2. at least 1 organ failure 3. belong to a subgroup with high short-term (28 day) mortality rate (>15%). Organ failure was defined based on a modified SOFA score adapted for patients with cirrhosis (CLIF-SOFA score)
The goals of the study were to assess the characteristics of cirrhotics that develop HE, describe the characteristics of HE in relation to the underlying liver disease (isolated decompensated cirrhosis or ACLF), identify risk factors for HE, and assess short-, mid- and long-term survival in relation to the presence or absence of HE and ACLF.

Patients and methods
• A total of 2145 successive patients were screened, FebruarySeptember 2011; of them 1348 were included in the Canonic Study • The majority (n = 1047) did not exhibit ACLF,while 301 subjects were diagnosed with ACLF. • A total of 460 patients exhibited HE at enrollment; the remaining 888 patients had no HE.

 The presence of HE was diagnosed as an impairment of cognition, consciousness, or motor function.  Severity of HE was assessed according to the West Haven scale and grouped in 2 levels (mild: grade I or II; severe: grade III or IV).

physical exam. gastrointestinal hemorrhage. hyponatremia or renal failure (at the time of enrollment). laboratory measurements. diuretic use. 90. competitive risk assessment). and 365 days following enrollment (adjusted by liver transplantation. . • Mortality at 28. and the presence of bacterial infections.Patients and methods • At enrollment we collected data from history. active alcoholism (> 14 drinks/week in women and > 21 drinks/week in men within 3 months). and causes of death were also recorded.

.Distribution of patients included in the study in relation to the presence of HE (left side) or ACLF (right side).

diabetes mellitus requiring treatment  Gender  Age .Hasil Patients with HE (n = 460) did not differ significantly from those without HE (n = 888) in relation to the causes:  Cirrhosis alcohol  Hepatitis C  Hepatitis C plus alcohol  Previous comorbidities: arterial hypertension.

ascites and overt HE  HE also exhibited a higher proportion of hospitalizations in the previous 3 months.Hasil  Patients with HE. there was a more frequent clinical history of previous decompensations. which was mainly due to higher number of hospitalizations related to HE and bacterial infections  There were no differences between patients with and without HE in the proportion of hospitalization during the previous 3 months for ascites or GI bleeding .

Patients with and without HE in the whole series .

which was higher in patients with HE.  HE patients had a higher prevalence of previous ascites and HE  Among precipitating events. and in the prevalence of gastrointestinal bleeding. which was lower in patients with HE. .Hasil Role of HE as an isolated decompensation  Patients without ACLF and with HE (n = 286) were slightly older than those without HE. differences were only found for the use of diuretics.

Hasil Role of HE as part of ACLF  Patients with ACLF and HE had no statistical differences in age to those without HE.  HE showed higher prevalence of previous HE and ascites.  The frequency of respiratory failure at enrollment was significantly higher in HE but affected less patients .

had less frequently alcoholic cirrhosis. and hyponatremia). and creatinine.  There were marked differences in the prevalence of precipitating events between non-ACLF (higher prevalence of diuretics) and ACLF (higher prevalence of bacterial infections. . ACLF patients show more abnormal inflammatory markers (leukocyte count and Creactive protein). INR.  Patients with ACLF had more deteriorated bilirubin.Hasil HE as an isolated decompensation or as part of ACLF  Patients with HE not associated with ACLF had significantly higher age. In addition. and had more frequently prior decompensations. active alcoholism. AST and less sodium.

. as part of ACLF and comparison between both.Role of HE as isolated decompensation.

Hasil Risk factors for HE and survival  Multivariate analysis assessing independent risk factors for HE in the whole series of patients and in those without ACLF found prior HE and diuretic use within the prior 3 months to be associated with the development of HE. only prior HE was significantly associated with current HE. .  In patients with ACLF.

independently of the presence or absence of HE .  The mortality probability of patients with ACLF was much higher than that of patients without ACLF.)  The mortality probability was significantly higher in patients with HE compared to those without HE. it increased significantly as the HE grade worsened.Hasil Risk factors for HE and survival (Cont.

Independent predicting factors for HE at enrolment .

INR. bilirubin. 90 days and 1 year in patients with HE at enrollment were age. sodium.)  In each subgroup (with and without ACLF) the mortality probability was significantly higher in patients with HE. The independent risk factors of mortality at 28 days. and creatinine .Hasil Risk factors for HE and survival (Cont.

Risk factors for short. . mid and long-term mortality in patients with HE.

1% and 5%). 34.4% of patients with HE and in 21.4%).2%).7% vs.5% vs.Hasil Risk factors for HE and survival (Cont.5% of patients without HE the cause of death could not be established . and hypovolemic shock (5.)  The main causes of death in patients with and without HE were multiorgan failure (36. septic shock (23.  In 20. a variety of other causes were present. 20.


etc. which lead to an increase in circulating toxins that impact the brain . renal failure. hyponatremia. acute liver damage.).Diskusi • Episodic HE is one of the most frequent complications of cirrhosis • Traditionally HE has been considered the effect on brain function of a combination of factors that include extrahepatic(infection. etc. gastrointestinal bleeding.) and intrahepatic mechanisms (worsening liver function.

We could not detect specific abnormalities caused by diuretic treatment . 3. development of HE is highly determined by the history prior to this complication. The most outstanding finding is the observation that previous HE is the most important risk factor for the development of HE  These data indicate that even in the most severe cases of cirrhosis. 2.Diskusi 1. This analysis indicates that the increase in HE with the use of diuretics was not explained by differences in the severity of liver failure. A second important finding is the poor relationship between the traditional precipitating factors and the development of HE.

. inactive drinkers (hepatitis C cirrhosis or alcoholic cirrhotics who stopped drinking).Diskusi From the results of our study we propose the existence of two presentations of HE: 1. 2. active alcoholism or dilutional hyponatremia. more frequently alcoholics as a consequence of impairment in liver function and bacterial infections. Isolated HE: occurs in older cirrhotics. HE associated with ACLF: occurs in young cirrhotics.

acute inflammatory reaction and organ failure(s) 4. characterized by severe liver failure. HE is not a homogeneous disorder 3.Kesimpulan 1. HE as a manifestation of ACLF. The relation of HE with prior history of HE supports the view that this is a highly recurrent disorder 2. A better characterization of the patient that develops HE will allow improvements in diagnosis and therapy of this severe complication. .


Kriteria Banevo V Back .

Back .

Back .

Back .

Back .

Back .