Budd-Chiari Syndrome is a rare disorder due to obstruction of hepatic venous outflow and generally follows a rapid fatal course. Hepatic vein thrombosis is a common complication with a high mortality rate and surgery for this condition is associated with a high perioperative mortality. Those who survive the acute phase almost invariably go on to develop cirrhosis of the liver and die within a few years from hepaic failure, bleeding esophageal varices or other complications of chronic liver disease. We have experienced the anesthetic management of three parients with Budd-Chiari syndrome who were treated with finger fracture and mesoatrial shunt. It is important that the anesthesiologist realizes that certain pathophysiological changes occur during the several surgical approaches to relieve the effect of hepatic vein obstruction, and perioper-ative hepatic dysfunction.
Budd-Chiari Syndrome* ; Esophageal and Gastric Varices ; Fibrosis ; Fingers ; Hemorrhage ; Hepatic Veins ; Humans ; Liver ; Liver Diseases ; Mortality

Liver cirrhosis patients are suffering from many complications, which are directly related to a poor prognosis. Although there have been many recent advances in diagnosis and treatment for varix and hepatic encephalopathy in cirrhotic patients, the standard practice for these conditions should consider the different medical resources and etiology of these liver diseases among various countries. The Korean Association for the Study of the Liver published in 2005 a clinical practice guideline for the treatment of cirrhosis complications, and this year, they revised the guideline for treating gastroesophageal varices and hepatic encephalopathy. This review summarizes the revised practice guideline and emphasizes the updated recommendation.
Diagnosis ; Esophageal and Gastric Varices ; Fibrosis ; Hepatic Encephalopathy ; Humans ; Liver Cirrhosis ; Liver Diseases ; Liver ; Prognosis ; Varicose Veins

Liver cirrhosis patients are suffering from many complications, which are directly related to a poor prognosis. Although there have been many recent advances in diagnosis and treatment for varix and hepatic encephalopathy in cirrhotic patients, the standard practice for these conditions should consider the different medical resources and etiology of these liver diseases among various countries. The Korean Association for the Study of the Liver published in 2005 a clinical practice guideline for the treatment of cirrhosis complications, and this year, they revised the guideline for treating gastroesophageal varices and hepatic encephalopathy. This review summarizes the revised practice guideline and emphasizes the updated recommendation.
Diagnosis ; Esophageal and Gastric Varices ; Fibrosis ; Hepatic Encephalopathy ; Humans ; Liver Cirrhosis ; Liver Diseases ; Liver ; Prognosis ; Varicose Veins

Chronic progressive liver diseases, such as liver cirrhosis, eventually cause portal hypertension & hepatic coma, and among the cause of death from UGI bleeding variceal bleeding secondary to portal hypertension is the most common, over 50%. Clinical management for variceal bleeding includes IV vasopressin injection, insertion of Balloon tamponade administration of somatosatin or propranolol, and shunt operation, but the effect has not been promising. (continue...)
Balloon Occlusion ; Cause of Death ; Esophageal and Gastric Varices* ; Hemorrhage* ; Hepatic Encephalopathy ; Hypertension, Portal ; Liver Cirrhosis ; Liver Diseases ; Propranolol ; Sclerotherapy* ; Vasopressins

PURPOSE: To evaluate the clinical significance of T1 high signal intensity on the globus pallidus as a predictor of severe hepatic encephalopathy in patients with acute-on-chronic liver failure (ACLF), which is a distinct syndrome characterized by multi-organ dysfunction including cerebral failure. MATERIALS AND METHODS: From January 2002 to April 2014, we retrospectively reviewed the magnetic resonance imaging (MRI) findings and clinical and magnetic resonance (MR) features of 74 consecutive patients (44 men and 30 women; mean age, 59.5 years) with liver cirrhosis. The chronic liver failure-sequential organ failure assessment score was used to diagnose ACLF. The pallidal index (PI), calculated by dividing the mean signal intensity of the globus pallidus by that of the subcortical frontal white matter were compared according to ACLF. The PI was compared with the Model for End-Stage Liver Disease (MELD) score in predicting the development of ACLF. RESULTS: Fifteen patients who were diagnosed with ACLF had higher hepatic encephalopathy grades (initial, P = 0.024; follow-up, P = 0.002), MELD scores (P < 0.001), and PI (P = 0.048). In the ACLF group, the mean PI in patients with cerebral failure was significantly higher than that in the patients without cerebral failure (1.33 vs. 1.20, P = 0.039). In patients with ACLF, the area under the curve (AUC) for PI was 0.680 (95% confidence intervals [CI], 0.52–0.85), which was significantly lower than that for the MELD score (AUC, 0.88; 95% CI, 0.77–0.99) (P = 0.04). CONCLUSION: The PI can be an ancillary biomarker for predicting the development of ACLF and severe hepatic encephalopathy.
Acute-On-Chronic Liver Failure ; Female ; Follow-Up Studies ; Globus Pallidus ; Hepatic Encephalopathy* ; Humans ; Liver Cirrhosis ; Liver Diseases* ; Liver* ; Magnetic Resonance Imaging ; Male ; Retrospective Studies ; White Matter

PURPOSE: To evaluate the clinical significance of T1 high signal intensity on the globus pallidus as a predictor of severe hepatic encephalopathy in patients with acute-on-chronic liver failure (ACLF), which is a distinct syndrome characterized by multi-organ dysfunction including cerebral failure. MATERIALS AND METHODS: From January 2002 to April 2014, we retrospectively reviewed the magnetic resonance imaging (MRI) findings and clinical and magnetic resonance (MR) features of 74 consecutive patients (44 men and 30 women; mean age, 59.5 years) with liver cirrhosis. The chronic liver failure-sequential organ failure assessment score was used to diagnose ACLF. The pallidal index (PI), calculated by dividing the mean signal intensity of the globus pallidus by that of the subcortical frontal white matter were compared according to ACLF. The PI was compared with the Model for End-Stage Liver Disease (MELD) score in predicting the development of ACLF. RESULTS: Fifteen patients who were diagnosed with ACLF had higher hepatic encephalopathy grades (initial, P = 0.024; follow-up, P = 0.002), MELD scores (P < 0.001), and PI (P = 0.048). In the ACLF group, the mean PI in patients with cerebral failure was significantly higher than that in the patients without cerebral failure (1.33 vs. 1.20, P = 0.039). In patients with ACLF, the area under the curve (AUC) for PI was 0.680 (95% confidence intervals [CI], 0.52–0.85), which was significantly lower than that for the MELD score (AUC, 0.88; 95% CI, 0.77–0.99) (P = 0.04). CONCLUSION: The PI can be an ancillary biomarker for predicting the development of ACLF and severe hepatic encephalopathy.
Acute-On-Chronic Liver Failure ; Female ; Follow-Up Studies ; Globus Pallidus ; Hepatic Encephalopathy* ; Humans ; Liver Cirrhosis ; Liver Diseases* ; Liver* ; Magnetic Resonance Imaging ; Male ; Retrospective Studies ; White Matter

BACKGROUND/AIMS: Thrombocytopenia is frequently found among patients with chronic liver disease, and its mechanism, especially among patients with decompensated liver cirrhosis had not been established. Therefore to elucidate the mechanism of thrombocytopenia, the relationship between thrombocytopenia and severity of hepatic dysfunction, splenomegaly was measured. We measured the peripheral blood components with splenic volume obtained from a computerized tomography of decompensated liver cirrhosis patients. METHODS: We studied 103 patients who had been diagnosed with decompensated liver cirrhosis with esophageal varices and ascites from January 1982 to August 1999. We checked their counts of platelets, albumin, bilirubin, splenic volume, degree of esophageal varices, hepatic encephalopathy and ascites by retrograde methods. RESULTS: In viral liver cirrhosis, thrombocytopenia and splenomegaly correlated well with disease severity but they didn't in alcoholic cirrhosis. Of special note, the platelet count was significantly lower and the splenic volume was larger in the Child C of viral cirrhosis patients group than in the alcoholic group(p<0.05). CONCLUSION: When we compared decompensated alcoholic with viral liver cirrhosis patients, the degrees of thrombocytopenia and splenomegaly were much less in the former group. The factors for this phenomena are Splenic Pooling theory, Platelet-associated IgG, Thrombopoietin and Toxic Marrow. We suggest that splenomegaly is an important factor among these, but the mechanisms involved in the pathogenesis of this hematologic phenomena are not completely understood. Especially in alcoholic liver cirrhosis, many other factors may be involved, including the direct effect of alcohol to bone marrow, so further studies will be needed to establish whether a causal relationship exists.
Alcoholics* ; Ascites ; Bilirubin ; Bone Marrow ; Child ; Esophageal and Gastric Varices ; Fibrosis ; Hepatic Encephalopathy ; Humans ; Immunoglobulin G ; Liver Cirrhosis* ; Liver Cirrhosis, Alcoholic ; Liver Diseases ; Liver* ; Platelet Count ; Splenomegaly ; Thrombocytopenia* ; Thrombopoietin

To evaluate the pathophysiology and surgical considerations for liver cirrhosis in the field of oral and maxillofacial surgery, 4 cases with maxillofacial traumas or infections in different stages of liver cirrhosis were reviewed. Although appropriate medical cares were ensured, 2 patients were died due to complications of the liver disease. Each cases were classified by the Pugh's classification system and analyzed with reference to laboratory findings and hospital courses. For improved understandings of pathophysiology of liver cirrhosis, the congulopathies, the lowered detoxification, the hepatic encephalopathy, the hepatorenal syndrome, the sepsis, other conditions-ascites, esophageal varix, portal hypertension, etc-and pre or postoperative complications were reviewed. And special emphases were made at the staging of liver cirrhosis in oral and maxillofacial surgery, preoperative preparations, and prevention of intraoperative or postoperative complications.
Classification ; Esophageal and Gastric Varices ; Hepatic Encephalopathy ; Hepatorenal Syndrome ; Humans ; Hypertension, Portal ; Liver Cirrhosis* ; Liver Diseases ; Liver* ; Postoperative Complications ; Sepsis ; Surgery, Oral*

BACKGROUND: The disturbances of portal circulation in chronic liver disease may cause hepatic failure, hepatic encephalopathy and variceal bleeding. The measure of porto-systemic shunt plays a significant role in the management and prognosis of the patients. So we have evaluated the relationship between the shunt index of thallium-201 liver scan and the histological grade and stage of chronic liver disease. METHODS: The thallium-201 scintigraphy per rectum was evaluated in 159 patients with chronic liver disease, which were proven with percutaneous liver biopsy. We used the heart to liver activity ratio at 20 minute as shunt index, representing portal-systemic shunt. The two pathologists scored independently hepatitis activity (lobular and porto-periportal activity) and stage (fibrosis). RESULTS: A significant difference was noted between the shunt index and the scores of fibrosis (p< 0.001) although this correlation was statistically weak (r=0.26, p=0.008). In cumulative logistic regression test, the shunt index had a effect on the fibrosis (p< 0.001) but not on the lobular and porto-periportal activity. Fibrosis was predicted as less than 2 if shunt index was less than 0.24, 3 if more than 0.24 but less than 0.46, 4 if more than 0.46. CONCLUSION: The shunt index of thallium-201 liver scintigraphy correlated only with fibrosis not with lobular and porto-periportal activity. As the fibrosis progresses in chronic liver disease, portal hypertension becomes more severe and the shunt index increases. Thallium-201 liver scan may be useful for evaluation of hepatic fibrosis instead of invasive liver biopsy in predicting the histological stage (fibrosis) of advanced chronic liver disease.
Biopsy* ; Esophageal and Gastric Varices ; Fibrosis ; Heart ; Hepatic Encephalopathy ; Hepatitis ; Humans ; Hypertension, Portal ; Liver Diseases* ; Liver Failure ; Liver* ; Logistic Models ; Prognosis ; Radionuclide Imaging* ; Rectum

Acute liver failure is a rare but fatal condition characterized by rapid deterioration of liver function resulting in coagulopathy and altered mentation in patients without known liver disease. The three most common causes of liver failure in Korea are hepatitis B virus, exposure to certain herbs, and hepatitis A virus. Because the cause of liver failure is the most important prognostic factor, the etiology of liver failure should be evaluated as the initial step in the assessment of affected patients. Patients with acute liver failure should be intensively monitored and treated for various secondary conditions that may occur or have already developed, including cerebral edema, seizures, hemodynamic instability, renal failure, infection, bleeding, and metabolic disturbances. Although treatment with N-acetylcysteine has shown a survival benefit in patients with mild hepatic encephalopathy, the overall mortality rate associated with acute liver failure is high unless patients undergo liver transplantation, prompting patients and physicians to be prepared for transplantation. Therefore, patients who are suspected to have, or who have been diagnosed with, acute liver failure should be transferred to a transplant facility and be prepared for liver transplantation while they undergo intensive monitoring and medical treatment.
Acetylcysteine ; Brain Edema ; Diagnosis ; Hemodynamics ; Hemorrhage ; Hepatic Encephalopathy ; Hepatitis A virus ; Hepatitis B virus ; Humans ; Korea ; Liver ; Liver Diseases ; Liver Failure ; Liver Failure, Acute* ; Liver Transplantation ; Mortality ; Renal Insufficiency ; Seizures