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대한간암연구학회지 2012년 제12권 2호; 120-127
간성뇌증의 관리 및 영양공급
인하대학교 의학전문대학원 소화기내과
이 진 우
Abstract
Nutrition and Management of Hepatic Encephalopathy
Jin-Woo Lee, M.D., Ph.D.
Department of Internal Medicine, Division of Gastroenterology and Hepatology, Inha University School of Medicine, Incheon, Korea
It has been estimated that at least 25% of patients with liver cirrhosis experience hepatic encephalopathy during the natural
history of the disease. Hepatic encephalopathy is more frequent in patients with more severe liver disease. Also, malnutrition is
common in patients with liver cirrhosis, and is considered a significant prognostic factor affecting quality of life, outcome, and
survival. Inadequate intake of nutrients, the hypermetabolic state, the diminished synthetic capacity of the liver and the impaired
absorption of nutrients are themain reasons that disrupt the metabolic balance in cirrhosis. In the general approach to cirrhotic
patients, the initial and most important step for the clinician is to recognize the extent of malnutrition. Unfortunately, the
Child-Pugh-Turcotte classification and the model for end-stage liver disease (MELD) do not include an assessment of nutritional
status in spite of the fact that malnutrition plays an important role in morbidity and mortality in end-stage liver failure. To date,
the practice of dietary protein restriction for patients with liver cirrhosis is deeply embedded among medical practitioners and
dietitians. However, the negative effects of protein restriction are clear, that is, increased protein catabolism, the release of amino
acids from the muscle, and possible worsening of hepatic encephalopathy. Nutritional support with sufficient protein
requirements, antioxidants, vitamins as well as probiotics may improve nutritional status, liver function, and hepatic
encephalopathy in patients with liver cirrhosis.
Key Words: Cirrhosis, Hepatic encephalopathy, Malnutrition, Nutrition
DEFINITION AND CAUSES OF HEPATIC disease (Table 1) (1,2).
ENCEPHALOPATHY The degree of mental status disturbance in hepatic ence-
phalopathy can be classified by the West-Haven criteria
Hepatic encephalopathy is a neuropsychiatric syndrome (Table 2) (3), ranges in a continuous extent that covers a
that follows liver dysfunction. Patients with hepatic ence- range from normal cognitive function (grade 0) to minimal
phalopathy can show various neurological illnesses such as hepatic encephalopathy (within grade 0) to overt hepatic en-
cognition and orientation disorders. Hepatic encephalopathy cephalopathy (grade 1-4).
is classified into 3 groups in according to the causative liver Minimal hepatic encephalopathy is a mild form of hepatic
❚책임저자 : 이진우
인천광역시 중구 인항로 27, 인하대병원 소화기내과(400-711)
Tel: 82-32-890-2548, Fax: 82-32-890-2549, E-mail: jin@inha.ac.kr
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이진우. 간성뇌증의 관리 및 영양공급
Table 1. Classification of hepatic encephalopathy (1)
Type Nomenclature Subcategory Subdivisions
A Encephalopathy associated with acute liver failure
B Encephalopathy associated with portal-systemic bypass and no intrinsic hepatocellular disease
C Encephalopathy associated with cirrhosis and portal hypertension/or systemic shunts Episodic HE Precipitated
Spontaneous
Recurrent
Persistent HE Mild
Severe
Treatment-dependent
Minimal HE
HE, hepatic encephalopathy.
Table 2. West Haven criteria for hepatic encephalopathy
Grade Consciousness Intellect and Behavior Neurologic Findings
0 Normal Normal Normal examination; if impaired psychomotor
testing then MHE
1 Mild lack of awareness Shortened attention span; impaired addition or subtraction Mild asterixis or tremor
2 Lethargic Disoriented; inappropriate behavior Obvious asterixis; slurred speech
3 Somnolent but arousable Gross disorientation; bizarre behavior Muscular rigidity and clonus; hyperreflexia
4 Coma Coma Decerebrate posturing
MHE, minimal hepatic encephalopathy.
encephalopathy that is defined as a cognitive dysfunction ty acids, false neurotransmitters, manganese, and gam-
presenting a abnormal psychometric tests without clinical ma-aminobutyric acid (7).
symptoms (1). Ammonia may originate from dietary proteins or the activ-
Pathophysiology of hepatic encephalopathy is still de- ity of intestinal urease or intestinal or renal glutaminase.
bated, and several theories have been proposed. Among Surprisingly, nearly 85% of total blood ammonia may be
them, the ammonia theory is the most widely-accepted and generated by intestinal glutamine deamination, whereas as
best-supported (4). little as 10-15% may originate from the deamination of pro-
The precise mechanisms underlying ammonia-induced teins by the gut macrobiota. Ammonia is metabolized by the
neurologic dysfunction have not been fully understood yet, liver, brain, muscle, and kidney (Fig. 1). The liver and mus-
but cerebral edema seems to be involved in this process. cle play central roles in ammonia detoxification by convert-
Glutamine (derived from glutamate and ammonia) is pro- ing it to urea (liver) and glutamine (liver and muscle). Under
duced within astrocytes in the brain. This glutamine attracts normal circumstances ammonia is detoxified in the liver. In
water and causes swelling of astrocytes (5). Ammonia can al- well-nourished patients with cirrhosis, the metabolic ca-
so directly cause oxidative stress in astrocytes, and it may pacity of the liver is exceeded resulting in an increase in cir-
lead to impaired intracellular signaling (6). culating ammonia. Under these circumstances the surplus
In addition to ammonia, other toxins implicated in the de- ammonia is detoxified in muscle with the production of glu-
velopment of hepatic encephalopathy include neurosteroids, tamine; this is in turn broken down to ammonia by gluta-
benzodiazepine-like molecules, mercaptans, short-chain fat- minase in enterocytes or else excreted by the kidney as am-
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대한간암연구학회지 2012년 제12권 2호
Fig. 1. Inter-organ ammonia metabolism in healthy individuals and in patients with cirrhosis (8).
monia however, in malnourished cirrhotic patients, the loss important factor is the presence of impaired digestion and
of muscle mass, commonly seen as a consequence of malnu- nutrient absorption due to portal hypertension, suggesting
trition, can adversely affect this alternative route of ammonia that controlling the pressure in the portal vein could improve
removal (8). the patients’ nutritional status (12). Cholestatic liver disease
Whether or not malnourished patients are more prone to is another reason for impaired absorption, especially of
develop hepatic encephalopathy has not been clearly estab- fat-soluble vitamins such as A,D,E and K, due to the reduced
lished, but could be anticipated based on several factors. intraluminal bile salt concentrations (14,15).
Malnutrition tends to be more common in patients with ad-
vanced liver disease, and hepatic encephalopathy is more 2. Increased energy expenditure and
likely in this group because inadequate dietary protein intake requirements
or low levels of BCAAs have a very deleterious effects on
hepatic encephalopathy (9). The systemic vasodilation and hyperdynamic circulation
in cirrhosis leads to a higher cardiac blood volume and
FACTORS CONTRIBUTING TO therefore a greater use of nutrients is a common cause of high
MALNUTRITION IN CIRRHOSIS energy expenditure and demand. Furthermore, the inability
of the damaged liver to clear activated proinflammatory
1. Inadequate dietary intake cytokines may promote an inflammatory response with an
increase in both energy expenditure and protein catabolism
The majority of cirrhotic patients unintentionally follow a (16). It has been suggested that elevated pro- and anti-in-
low caloric diet, a fact that is attributed to various side-effects flammatory cytokine levels have the potential to result in hy-
observed in cirrhosis. Loss of appetite or alcohol-induced permetabolism in cirrhosis (17,18).
anorexia, are the most common reasons. Also, early satiety
due to impaired gastric accommodation (10,11) and impaired 3. Diminished synthesis or absorption of
expansion capacity of the stomach due to the presence of nutrients
clinically evident ascites (12) quite often lead to an inade-
quate nutrient intake. Patients with chronic liver diseases Other important factors in the loss of body protein are the
experience abdominal pain, nausea and bloating and are inadequate synthesis of various proteins from the affected
found to have altered gut motility, all of which lead to the liver, the diminished storage capacity of the cirrhotic liver
development of functional dyspepsia (13). One other and an impaired absorption of nutrients from the portal
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이진우. 간성뇌증의 관리 및 영양공급
hypertensive enteropathy. tus and severity of disease in cirrhotic patients are the Child-
After an overnight fast, an early switch to gluconeogenesis Pugh-Turcotte classification and the model for end-stage
from amino acids originating from body proteins is often liver disease (MELD). Unfortunately, these systems do not
among cirrhotic patients. The lack of sufficient amounts of include an assessment of nutritional status in spite of the fact
hepatic glycogen reserves, due to the impaired synthetic that malnutrition plays an important role in morbidity and
capacity of hepatic cells, results in the mobilization of amino mortality in liver cirrhosis.
acids from the skeletal muscles so that the proper amount of The use of anthropometric parameters which are not
glucose is provided. This condition is observed in healthy affected by the presence of ascites or peripheral edema has
individuals after a fasting period of approximately 3 days also been recommended (24,25). Such parameters include
(19,20). mid-arm muscle circumference (MAMC), mid-arm circum-
Other conditions such as altered intestinal flora and lesser ference (MAC), and triceps skin fold thickness (TST).
synthesis and secretion of bile salts and pancreatic enzymes Diagnosis of malnutrition is established by values of MAMC
are also significant causes of nutrient loss. and/or TST below the 5th percentile in patients aged 18-74
years, or the 10th percentile in patients aged over 74 years
DIAGNOSIS OF HEPATIC (26).
ENCEPHALOPATHY BMI changes may afford a reliable indicator of malnu-
trition using different BMI cutoff values depending on the
Hepatic encephalopathy is generally accompanied by presence and severity of ascites; patients with a BMI below
advanced liver disease; therefore, muscle weakness, jaun- 22 with no ascites, below 23 with mild ascites, or below 25
dice, ascites, palmar erythema, edema, spider telangiectasias, with tense ascites are considered to be malnourished (26).
and fetor hepaticus can be noted on physical examination. However, a standardized simple and accurate method for
Clinicians should check for gastrointestinal hemorrhage, evaluating malnutrition in cirrhosis remains to be
uremia, use of anti-psychotics or diuretics, protein hyper- established.
ingestion, infection, constipation, dehydration, electrolyte
imbalance, etc (21). Common symptoms include concen- TREATMENT OF HEPATIC
tration disorders, sleep disorders, and movement disorders, ENCEPHALOPATHY
including lethargy or coma.
Venous levels of ammonia are not helpful because they The goal of treatment is to prevent secondary damage
are not proportional to the severity of hepatic encephalop- caused by decreased consciousness, normalize the patient's
athy and some patients with sever hepatic encephalopathy state of consciousness, prevent recurrence, and to improve
have normal venous ammonia levels (22). the prognosis and quality of life by eliminating the social and
Brain MRI is considered better than brain CT in the diag- economic restrictions caused by hepatic encephalopathy. The
nosis of brain edema accompanying hepatic failure, but this precipitating factor can be identified in more than 80%
is not true for hepatic encephalopathy. Brain CT is useful of patients with hepatic encephalopathy (21). The currently
when differentiating between organic causes of neuropsychi- known precipitating factors of hepatic encephalopathy and
atric disorders such as intracranial hemorrhage (23). the corresponding tests and treatments are shown in Table 3
(27).
ASSESSMENT OF NUTRITIONAL STATUS
IN END-STAGE LIVER DISEASE (ESLD) 1. Medications
Generally accepted methods for assessing the clinical sta- The primary treatment of hepatic encephalopathy is non-
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