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- Review Article Nutritional Management in Patients with Liver Dysfunction
- Tae Hee Lee, M.D.
- 간기능 부전환자에서의 영양관리
- 이태 희, M.D.
-
Surgical Metabolism and Nutrition 2017;8(1):1-6.
DOI: https://doi.org/10.18858/smn.2017.8.1.1
Published online: June 30, 2017
Division of Gastroenteroloy and Hepatology, Department of Internal Medicine, Konyang University College of Medicine, Daejeon, Korea
- Correspondence to: Tae Hee Lee, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Konyang University College of Medicine, 158 Gwanjeodong-ro, Seo-gu, Daejeon 35365, Korea Tel: +82-42-600-9370, Fax: +82-42-600-9090, E-mail: green740@naver.com
• Received: June 4, 2017 • Accepted: June 21, 2017
Copyright: © The Korean Society of Surgical Metabolism and Nutrition
This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Abstract
- Liver disease and nutritional status are known to affect each other. When liver disease is severe, patients become more malnourished and have a worse prognosis. Adequate nutritional support for patients with liver diseases can improve a patient’s condition and prognosis. In acute liver failure, malnutrition is uncommon, and the disease prognosis is determined within a short time. Patients with acute liver failure may survive and recover if they receive a transplant. Considerations should be given to the management of glucose intolerance and hyperammonemia. However, well-designed clinical trials are still lacking until now. In the case of liver cirrhosis, malnutrition may occur due to a variety of causes, and as in other diseases, oral or enteral nutrition is preferred to parenteral nutrition. Even if esophageal varices are present, it is possible to install a feeding tube. However, in the presence of ascites, PEG (percutaneous endoscopic gastrostomy) becomes contraindicated due to risk of complications. Calorie intake of 30~35 Kcal/kg/day and protein intake of 1.2 to 1.5 g/kg/day are appropriate. Protein restriction should not be necessary unless hepatic encephalopathy is severe. Late evening snacking and intake of branched chain amino acids can be helpful.
급성간부전(Acute liver failure)의 영양관리
대부분의 급성간부전 환자는 영양상태가 좋은 편이다. 주된 문제는 간성혼수와 뇌부종에 의한 사망이다. 질환자체가 짧은 시간 진행하여 신속히 재생되거나 이식하지 못하면 사망할 수 있어 아직까지는 중개 연구는 없는 상태이다.
유럽에서의 관찰 연구가 두 편 있다. 하나는 2004년 발표된 연구로 11개국 33개 간질환 중환자실에 설문조사 하였다.[1] 25개 중환자실에서 정맥영양을 사용하였고 8개 중환자실에서는 표준식이를 사용하는 경장영양을 선호하였다. 정주 포도당은 중앙값 4 g/kg/d로 공급하였고 지방 정주는 몇몇 에서만 0.9∼1.0 g/kg/d로 이루어졌다. 아미노산 용액은 주로 분지쇄아미노산(BCAA)이 풍부한 용액을 사용하였고 0.9∼1.0 g/kg/d로 공급하였다. 약 50% 환자는 경장영양을 받았고 정맥영양의 경우 다양한 주입속도와 혈중 농도를 보였다
두 번째 연구는 2016년에 발표된 것으로 11개국 22개 이식센터에 설문하였다.[2] 환자는 24시간 이내 특수병동에 입원하여 다학제 진료를 받았고 중환자 진료와 유사하였다. 80% 이상의 센터에서 아세트아미노펜에 의하지 않은 급성간부전환자에게 N-acetyl-cysteine을 투여하였다. ICP monitoring은 12센터에서 이루어 졌고 대부분 환자의 이식대기시간은 1∼2일이었다. 90일 생존률은 76%였고 응급간이식은 36%에서 이루어졌고 42%는 내과적 치료만으로도 회복하였다. 영양관리는 병동과 중환자실에 차이가 있었는데 73% 센터에서는 절반이상의 환자들에서 그리고 23% 센터에서는 항상 비위관을 통한 영양공급을 한다고 하였고 병동에서는 소수의 환자들에만 비위관을 사용하였다. 78% 센터에서는 정맥영양을 50% 미만의 환자에게 사용하였고 BCAA는 거의 사용하지 않는다고 하였다.
급성간부전에서는 당불내성을 보이는데 혈청 인슐린과 C-peptide 농도가 10배가량 증가하고 인슐린 감수성도 대조군의 15% 정도로 감소한다고 알려져 있다. 또한 글루카곤 농도도 50배가량 증가하며 포도당 주입에 반응하지 않는 것으로 알려져 있다.[3] 혈청 유리지방산과 케톤체의 농도가 낮아 간내 케톤생성이 거의 없다는 것을 의미한다.[4] 아미노산의 경우에는 3∼4배 증가하는데 상대적으로 트립토판과 방향족 아미노산이 증가하고 BCAA는 감소하는 것으로 알려져 있다. 또한 근육과 뇌에서 글루타민이 암모니아와 알라닌으로 전환되어 암모니아의 농도도 증가하여 뇌부종의 원인이 될 수 있다.[5,6]
유럽대사영양학회에서는 급성간부전환자의 정맥영양에 대해 5∼7일에 정상적인 경구 섭취가 불가능할 때 영양치료를 시작하기를 권하고 있다. 또한 개개인의 에너지 소비를 측정하기 위해 간접열량계를 사용하고 포도당과 지질을 동시 투여하고 혈당과 암모니아에 대해 모니터링하라고 권고하고 있다(Table 1).[7] 추후 질병 경과가 짧은 급성 간부전 환자를 대상으로 한 전향적인 연구가 꼭 필요하다. 한편 만성 간질환의 급성 악화 경우(Acute-on-chronic liver failure)에도 영양 치료 역할이 규명되어야 할 것이다.
Table 1
Summary of statements: acute liver failure (parenteral nutrition)
만성간질환(Chronic liver disease)의 영양관리(성인 간경변을 중심으로)
원래의 Child-Turcotte score에는 하나의 변수로 영양이 들어있었고 예후인자로 알려져 왔다.[8]
영양선별의 방법으로는 다양한 방법들이 소개되어 있는데 각각의 장단점이 있고 적용환경이 다르므로 유의해서 사용하여야 한다(Table 2).[9] 영양평가의 경우에는 통상적으로 사용하는 CPT score와 MELD score 이외에도 anthropometry, subjective global assessment, handgrip assessment, biochemistry (Vitamin, Zn), 포함 골밀도 등을 사용할 수 있다.[10]
Table 2
Summary of nutrition screening tools
APACHE II = Acute Physiology and Chronic Health Evaluation II; CNST = Canadian Nutrition Screening Tool; GI = gastrointestinal; MNA = Mini Nutritional Assessment; MST = Malnutrition Screening Tool; MUST = Malnutrition Universal Screening Tool; NRS-2002 = Nutritional Risk Screening 2002; NUTRIC = Nutrition Risk in Critically Ill; SNAQ = Short Nutritional Assessment Questionnaire; SOFA = Sequential Organ Failure Assessment.
간경변 환자에서의 영양불량의 빈도는 간기능에 따라 다르며 Child A의 경우 보통 20%, Child B는 25∼40%, Child C는 44∼90%가량 된다고 알려져 있으며 특히 간이식 대기자들은 모두가 영양불량을 가진다고 보고하였다.[11-13]
Table 3
Causes of malnutrition in cirrhosis
영양불량과 관련된 임상성적은 다음의 표에 정리하였다(Table 4).[15] 근감소증이 사망률과 관계가 있었고 영양불량이 세균감영의 위험을 증가시키고 간성뇌증의 발생, 수혈 요구도, 술후 입원기간을 더 연장시켰다고 하였다.
Table 4
Studies of outcomes associated with malnutrition in end stage liver disease
한편 중재를 통한 임상성적의 향상의 그 연구수가 제한적이며 다음과 같은 결과를 보였다(Table 5).[16] 술전 정맥영양은 복수발생을 감소시켰고 감염, 술후 합병증, 술후 폐렴을 감소시켰으나 경장영양은 아직 유효성을 입증하지 못하였다. 한편 영양보충으로 간경변 환자의 간성뇌증의 개선을 보였고 간세포암 환자에서 복수의 발생을 감소시켰다고 보고하였다.
Table 5
Results of meta-analysis of parenteral nutrition, enteral nutrition and supplements
간경변에서의 대사이상은 다음그림에 요약하였다(Fig. 1). 간세포의 수가 줄면 식이 중 포도당의 소비가 줄고 글리코겐의 합성도 줄어들게 되어 식후 혈당이 더 증가하고 그에 따라 췌장에서 인슐린분비도 증가하여 말초조직에서 인슐린 저항성이 나타나고 당불내성이 발생하게 된다. 한편 금식기간에는 에너지 부족이 쉽게 발생하여 지방을 이용하여 유리지방산과 케톤체를 증가시키고 단백이화작용이 나타나서 저단백혈증, 근감소증, 음의 질소균형을 보이게 된다.[17]
간경변환자의 영양관리는 다음 표에 정리하였다(Table 6). 간경변환자는 금식에 취약하여 12시간의 금식은 보통사람 수일의 금식에 해당할 수 있어 당장 포도당 주입을 시작하여야 하고 72시간 이상 금식한다면 정맥영양을 시작해야 한다.[7] 사용가능 하다면 필요한 열량의 측정을 위해서는 간접열량계 사용을 추천한다.[18] 전체 열량은 30∼40 Kcal/kg/day 정도로 탄수화물은 비단백열량의 50∼60%를 공급하고 지방은 40∼50%, 단백질은 대상성 간경변의 경우에는 1.2 kg/kg/day, 비대상성 간경변의 경우는 1.5 kg/kg/day까지 공급하는 것을 추천한다.[19] 미량원소도 매일 공급하고 re-feeding syndrome은 꼭 주의하여야 한다.[7] 가느다란 비위관의 경우 식도정맥류가 있어도 금기는 아니나 경피위루술은 합병증의 위험이 높아 추천되지 않는다.[20] 밤 9시 이후의 야식이 도움이 될 수 있는데 당신생을 억제하고 지방의 분해도 억제하는 효과가 있어 1989년부터 다양하게 시도되고 있다.[21] BCAA는 근육과 뇌에서 대사되는데 단백합성을 촉진하고 이화를 억제하며 당신생의 기질로 사용되기도 하여[22] 1년간 또는 2년간의 장기 투여로 event-free rate와 간부전의 위험, 간성뇌증, 혈청 알부민치를 개선시켰으나 사망률을 줄이지는 못하였다.[23-26]
Table 6
Summary of nutritional support in the patients with liver cirrhosis
간경변증은 간실질세포의 감소와 그에 따른 대사장애로 인슐린 저항성, 지방과 단백의 이화가 심하게 일어나고 영양불량에 취약하며 다양한 방법으로 영양선별 및 평가를 해야 한다. 열량은 re-feeding syndrome에 주의하며 충분히 공급하고 단백 제한을 하지 말아야 한다. 야식과 분지쇄 아미노산이 도움이 될 수 있다. 중재를 통한 임상 연구가 아직도 부족한 상태이므로 향후 추가 연구가 절실히 필요하다.
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Fig. 1
Metabolic derangement of liver cirrhosis.
Fig. 1
Nutritional Management in Patients with Liver Dysfunction
Summary of statements: acute liver failure (parenteral nutrition)
| Subject | Recommendations | Grade |
|---|---|---|
| General | Commence artificial nutrition when patient is unlikely to resume normal oral nutrition within the next 5∼7 days. | C |
| Use parenteral nutrition when patients cannot be fed adequately by enteral nutrition. | ||
| Energy | Provide energy to cover 1.3×REE (resting energy expenditure). | C |
| Consider using indirect calorimetry to measure individual energy expenditure. | ||
| Give i.v. glucose (2∼3 g/kg/d) for prophylaxis or treatment of hypoglycaemia. In case of hyperglycaemia, reduce glucose infusion rate to 2∼3 g/kg/d and consider the use of i.v. insulin. | ||
| Consider using lipid (0.8∼1.2 g/kg/d) together with glucose to cover energy needs in the presence of insulin resistance. | ||
| Amino acids | In acute or subacute liver failure, provide amino acids at 0.8∼1.2 g/kg/d. | C |
| Monitoring | Employ repeat blood sugar determinations in order to detect hypoglycaemia and to avoid PN related hyperglycaemia. | C |
| Employ repeat blood ammonia determinations in order to adjust amino acid provision. |
Summary of nutrition screening tools
| Screening tool _(care setting ) | Advantages | Disadvantages | Tool components |
|---|---|---|---|
| MUST _(community) | High interrater reliability Content and predictive validity for length of hospital stay and mortality Practical |
Weight from fluid collections (ascites, peripheral edema) not accounted Disease severity not considered |
BMI Unplanned weight loss in past 3-6 months Acutely ill and unable to eat for ≥5 days |
| NRS-2002 _(hospital) | Content and predictive validity Moderately reliable Practical Considers disease severity |
Weight from fluid collections (ascites, peripheral edema) not accounted | Weight loss Food intake BMI Disease severity |
| NUTRIC _(critically ill) | Externally validated (n≥1,000 patients) | Interleukin-6 not widely available Requires training Classic nutrition parameters not considered |
Age APACHE II and SOFA scores Comorbidities Days in hospital pre-ICU Interleukin-6 |
| MNA _(elderly [home-care programs, nursing homes, and hospitals]) | Includes physical and mental components plus dietary questionnaire Predictive validity for adverse outcome, social functioning, mortality, and doctor visits Practical |
Content validity not reported Interrater reliability modest Weight from fluid collections (ascites, peripheral edema) not accounted Disease severity not considered |
GI symptoms Weight loss Mobility Psychological stress/acute disease Neuropsychological problems BMI |
| SNAQ _(hospital) | Simple/practical Facilitates identification and treatment of malnourished inpatients |
Weight from fluid collections (ascites, peripheral edema) not accounted Disease severity not considered |
Unintentional weight loss Decreased appetite Use of supplements or tube feeding |
| MST _(hospital) | Simple/practical Predictive validity for length of stay Excellent reliability Highly sensitive |
Weight from fluid collections (ascites, peripheral edema) not accounted Disease severity not considered | Unintentional weight loss Quantity of weight lost Decreased appetite |
| RFH-NPT _(ambulatory hospital) | Simple/practical Cirrhosis-specific features Excellent intraobserver and interobserver reproducibility Good external validity Predictive of clinical deterioration and transplant-free survival |
Valid in population with cirrhosis only Impact of nutritional therapy based on screening score unknown | Alcoholic hepatitis or tube feeding Considers fluid overload Dietary intake reduction Weight loss+option for assessing diuretic use |
| CNST _(hospital) | Simple/practical Validated against SGA (sensitivity 67∼73%, specificity 80∼86%) High reliability |
Weight from fluid collections (ascites, peripheral edema) not accounted Disease severity not considered Symptoms not considered | Unintentional weight loss Dietary reduction |
APACHE II = Acute Physiology and Chronic Health Evaluation II; CNST = Canadian Nutrition Screening Tool; GI = gastrointestinal; MNA = Mini Nutritional Assessment; MST = Malnutrition Screening Tool; MUST = Malnutrition Universal Screening Tool; NRS-2002 = Nutritional Risk Screening 2002; NUTRIC = Nutrition Risk in Critically Ill; SNAQ = Short Nutritional Assessment Questionnaire; SOFA = Sequential Organ Failure Assessment.
Causes of malnutrition in cirrhosis
| Decrease in oral intake | • Anorexia (↑TNF- α &leptin) |
| • Nausea | |
| • Vomiting | |
| • Early satiety (cholecystokinin) | |
| • Taste abnormalities (Zn, Mg def.) | |
| • Alcohol abuse | |
| • Medications | |
| • Iatrogenic (restrictive diet, NPO) | |
| Maldigestion and malabsorption | • Fat malabsorption (cholestasis, chronic pancreatitis) |
| • Water-soluble vitamin malabsorption (alcohol abuse) | |
| • Calcium and lipid-soluble vitamin malabsorption (cholestasis) | |
| • Bacterial overgrowth | |
| • Portal hypertensive enteropathy | |
| Associated renal disease | • Urinary micronutrient losses |
| • Hepatorenal syndrome | |
| • Viral hepatitis associated glomerulonephritis (MGN, MPGN) | |
| Metabolic abnormalities | • Glucose intolerance |
| • Increased protein and lipid catabolism (similar to sepsis) | |
| • Trauma or other catabolic status |
Studies of outcomes associated with malnutrition in end stage liver disease
| Reference | No. of subjects, cohort studied | Outcome |
|---|---|---|
| Tandon et al, Liver Transpl, 2012 | 142, listed for LT | Sarcopenia was an independent predictor of mortality (HR, 2.4). |
| Alberino et al, Nutrition, 2001 | 212, hospitalized | Sarcopenia and loss of fat mass were independent predictors of mortality (HR, +0.8 and +2.0, respectively, compared with HR for mortality based on Child-Pugh score alone). |
| Muller et al, Hepatology, 1992 | 123, listed for LT | Decreased body cell mass prior to liver transplantation is associated with increased posttransplant mortality (3.2-fold). |
| Merli et al, Clin Gastroenterol Hepatol, 2010 | 150 | Protein malnutrition (MAMC <5th percentile) associated with increased risk of bacterial infections. |
| Huisman et al, Eur J Gastroenterol Hepatol, 2011 | 84 | Malnutrition independently associated with encephalopathy and spontaneous bacterial peritonitis (OR, 4.2). |
| Stephenson et al, Transplantation, 2001 | 99, listed for LT | Malnutrition at the time of liver transplant associated with increased transfusion requirements and increased postoperative hospital stay. |
Results of meta-analysis of parenteral nutrition, enteral nutrition and supplements
| Outcomes | Parenteral nutrition | Enteral nutrition | Supplements | |||||
|---|---|---|---|---|---|---|---|---|
| LT | Surgery | LC | LT | LC | HCC | LT | Surgery | |
| Mortality | 0.42 (3) | 0.46 (3) | 0.85 (4) | No data | 0.53 (5) | 1.18 (4) | 0.27 (1) | 1.50 (3) |
| Ascites+ | No data | 0.65 (2) | No data | No data | 0.72 (2) | 0.53 (2) | No data | No data |
| Ascites− | No data | No data | 0.86 (1) | No data | 4.16 (2) | No data | No data | No data |
| GI bleeding | No data | 2.82 (1) | 1.17 (4) | No data | 0.87 (3) | 1.50 (2) | No data | 1.10 (1) |
| HE+ | No data | 0.66 (2) | 3.13 (2) | 1.17 (1) | 0.87 (9) | 0.75 (2) | 0.43 (1) | N/A |
| HE− | No data | No data | No data | No data | 3.75 (2) | No data | No data | No data |
| Infections | 0.55 (1) | 0.47 (1) | 0.91 (4) | 0.46 (1) | 0.50 (3) | 0.35 (1) | No data | 0.86 (3) |
| Serum bilirubin | 1.86 (2) | 0.30 (1) | 0.37 (2) | No data | 0.24 (2) | No data | No data | No data |
| LOS | 7.20 (1) | No data | 1.08 (2) | −9.80 (1) | −8.00 (1) | - | No data | - |
| Total Postop. Cx | No data | 0.63 (1) | N/A | No data | N/A | N/A | No data | 0.85 (4) |
| Intra-abd. Cx | No data | 1.01 (1) | N/A | No data | N/A | N/A | No data | 0.30 (2) |
| Postop pneumonia | No data | 0.31 (1) | N/A | No data | N/A | N/A | No data | 0.55 (2) |
| Postop wound infection | No data | 0.63 (1) | N/A | No data | N/A | N/A | No data | 0.77 (2) |
LT = liver transplantation; LC = liver cirrhosis; HCC = hepatocellular carcinoma; HE+ = development of hepatic encephalopathy; HE- = improvement of hepatic encephalopathy; LOS = length of stay; N/A = not available; Cx = complication.
Summary of nutritional support in the patients with liver cirrhosis
| • Stepwise approach: counseling, supplements, tube feeding, parenteral nutrition |
| • Ensure adequate energy intake (total energy 30∼35 Kcal/kg/day, non-protein energy 25 Kcal/kg/day) |
| • Use indirect calorimetry if available |
| • Provide enough protein (1.2∼1.5 g/kg/day) without restricting it |
| • Use branched chain amino acids after GI bleeding and in HE grade 3/4 |
| • Use fat as fuel (recommended ratio n6:n3=2:1) |
| • Avoid re-feeding syndrome |
| • Frequent meals including late evening snack (PM9∼AM7) |
Table 1 Summary of statements: acute liver failure (parenteral nutrition)
Table 2 Summary of nutrition screening tools
APACHE II = Acute Physiology and Chronic Health Evaluation II; CNST = Canadian Nutrition Screening Tool; GI = gastrointestinal; MNA = Mini Nutritional Assessment; MST = Malnutrition Screening Tool; MUST = Malnutrition Universal Screening Tool; NRS-2002 = Nutritional Risk Screening 2002; NUTRIC = Nutrition Risk in Critically Ill; SNAQ = Short Nutritional Assessment Questionnaire; SOFA = Sequential Organ Failure Assessment.
Table 3 Causes of malnutrition in cirrhosis
Table 4 Studies of outcomes associated with malnutrition in end stage liver disease
Table 5 Results of meta-analysis of parenteral nutrition, enteral nutrition and supplements
LT = liver transplantation; LC = liver cirrhosis; HCC = hepatocellular carcinoma; HE+ = development of hepatic encephalopathy; HE- = improvement
of hepatic encephalopathy; LOS = length of stay; N/A = not available; Cx = complication.
Table 6 Summary of nutritional support in the patients with liver cirrhosis
