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1 103PG 4PG Course 2012 Portal Hypertension Hepatic EncephalopathyHyung Joon KimDepartment of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, KoreaHepatic encephalopathy is one of the most important clinical manifestations in decompensated liver cirrhosis. Clinical manifestations are multiple and varied, ranging from minimal neurological changes to coma. Ammonia is the main toxic substance involved in the pathogenesis of hepatic encephalopathy, although other mechanisms, such as modifications of the blood-brain barrier, disruptions in neurotransmission and abnormalities in GABA ergic and benzodiazepine pathways may also play a role. The identification and treatment of precipitating factors is crucial in the management of patients with hepatic encephalopathy. Current treatments are based on reducing intestinal ammonia load by agents such as antibiotics or disaccharides, although their efficacy is yet.

2 In spite of improved therapeutic options for encephalopathy, the long-term survival is still low. Thus, hepatic encephalopathy remains a serious complication of liver cirrhosis. Establishment of truly effective prevention modalities and broader application of liver transplantation will help rescue patients suffering from this complication of liver cirrhosis in the near future. , , , . , 3 . : , . , .. , - .1 . , 1 42% , 3 23% .2.

3 Postgraduate Course 2012104 .3-7 . phenol, mercaptan . , , , GABA benzodiazepine . , , .1. , .8 . , .9 , .. MRI , .10 spectroscopy positron emission tomography , .2.. ,11 , mercaptane.

4 3 . (1) , . , . , .. 2-8 . (2) , , , ( , , ). Krebs-Henseleit . - 105 , , , .. (1) alphaketoglutaric .. (a) alphaketoglutaric acid + ammonia glutamic acid (b) glutamic acid + ammonia glutamine alphaketoglutaric acid , glutamic acid Krebs alphaketoglutaric acid .3,12 (2) Krebs pyruvic acid (3) alphaketoglutaric acid glutamine ATP.

5 , . 90% .13 .14 , . , , .15 , . , . mercaptan .16 Mercaptan mercaptan . , mercaptan .. mercaptan , .173. 4.

6 3,181) False neurotransmitter theory Fischer Baldessarini 1971 .19 .. valine, leucine, isoleucine . , Postgraduate Course 2012106 (aromatic) (tryptophan, phenylalanine, tyrosine, dopamine norepinephrine ) .20 , , . phenylalanine tyrosine 3 hydroxylase . tyramine, octopamine, serotonin beta-phenylethanolamine (false neurotransmitter) . dopamine norepinephrine catecholaminergic .21 , .22-25 (1) octopamine catecholamine.

7 (2) norepinephrine dopamine . (3) . (4) bromocriptine .2) GABA ergic theoryGABA chloride . GABA GABA , .26 GABA GABA , , . GABA benzodiazepine . GABA , (hyperpolarization) .3) Benzodiazepine theory GABA ,27,28 benzodiazepine GABA . , benzodiazepine .4).

8 29, 30 , glutamate , . : . 107 Table 1. HE typeN om enclatureSubcategorySubdivisionsAEncepha lopathy associated with acute liver failure BEncephalopathy associated with portal-systemic bypass and no intrinsic hepatocellular disease CEncephalopathy associated with cirrhosis and portal hypertenstion/or systemic shuntsEpisodic HEPrecipitatedSpontaneousRecurrentPersis tent HEMild SevereTreatment-dependentMinimal HE HE, hepatic encephalopathy , , Ferenci 2002 , 3 .31 (1) Type A, (2) Type B, (3) Type C, ( , ) Type C (episodic), (persistent) (minimal) (Table 1).

9 , . 2 .32,33 , 8% .34 Child-Pugh class A 40% .35 , , , , (palmar erythema), , (spider telangiectasias), (fetor hepaticus) . , , Postgraduate Course 2012108 Table 3. West Haven CriteriaGradeConsciousnessIntellect and BehaviorNeurologic Findings0 NormalNormalNormal examination;if im paired psychom otor testing then MHE1 Mild lack of awarenessShortened attention span; impaired addition or subtractionM ild asterixis or trem or2 LethargicDisoriented; inappropriate behaviorObvious asterixis; slurred speech3 Somnolent but arousableGross disorientation; bizzare behaviorMuscular rigidity and clonus; hyperreflexia 4 ComaComaDecerebrate posturingMHE, minimal hepatic 2.

10 M ain precipitating factors of hepatic encephalopathy according to their possible m echanismIncrease in nitrogen loadG astrointestinal bleedingExcessive dietary protein intakeHyperazotaemiaConstipationRenal failureMetabolic disordersH yponatraem ia (astrocyte swelling)Hypokalaemia (increase in renal NH3)Metabolic alkalosis (increase in NH3 diffusion across the blood--brain barrier)HypoxemiaHypovolemiaDehydration (diuretics, diarrhea)MedicationN arcoticsBenzodiapezinesSedativesD iuretics (protein catabolism )MiscellaneousBacterial infectionSurgery (protein catabolism)Additional concomitant acute liver dysfunction (viral, drug-induced, acutealcoholic hepatitis)Progressively worsening liver diseaseTransjugular intrahepatic portosystemic shuntNH3, ammonia. West-Haven criteria (Table 3).