Curriculum Vitae

Nama : dr Azzaki Abubakar, SpPD, KGEH

Tempat dan tgl lahir : Banda Aceh 29 Juli 1971
Status : Menikah (istri dr. Yusnidar, M.Epid, anak : Salman Asyi)

Riwayat Pekerjaan :
1.Dokter Puskesmas Padang Panjang, Aceh Barat, 1999 -2000
2. Puskesmas Alue Bilie Aceh Barat 2000-2001
3. Staf Divisi Gastro Entero Hepatologi 2003 - sekarang
4. Kepala Instalasi Endoskopi RSUD DR. Zainoel Abidin, 2008 sekarang
5. Ketua Komite Mutu dan Keselamatan Pasien RSUD Dr. Zainoel Abidin Banda Aceh, 2014-sekarang
6. Assesor LAM PT Kes

Riwayat Pendidikan :
1. SD 16, SMP 1, SMA 3 (Banda Aceh)
2. FK Universitas Syiah Kuala Banda Aceh, 1990-1998
3. Internist, FK Universitas Diponegoro Semarang, 2003-2008.
4. Konsultan Gastroenterohepatologi, FK Universitas Indonesia Jakarta, 2013

Riwayat Training :
1. Basic Endoskopic Training, RSCM FK Universitas Indonesia, Jakarta 2009
2. USG di LP Puski Jakarta 2008
3. Workshop Endoscopic Ultrasound Jakarta 2015, Surabaya 2016
4. Advanced Endoscopy Training, Kobe Japan 2016
5. Pelatihan Patient Safety dan Insiden Keselamatan Pasien PERSI, Jakarta 2016
 NUTRITION MANAGEMENT
IN LIVER DISEASE

Dr. Azzaki Abubakar, SpPD-KGEH

Gastroenterohepatology Division Internal Medicine Department
Syiah Kuala University/Dr. Zainoel Abidin General Teaching Hospital
 INTRODUCTION

Nutrition and liver disease have close

interrelationship
Clinician are frequently focus on
pharmacologic therapy rather than
nutrition management
Appropriate nutritional therapy could reduce
morbidity and mortality
 LEARNING TOPICS
Nutritional problem in chronic liver disease
Nutrient metabolism in Liver Diseases
Alteration of metabolic status in Chronic Liver
Diseases (CLD)
Malnutrition related to CLD
Strategy of nutrition management in CLD
Advantage and disadvantage of Enteral and
Parenteral nutrition for CLD
Nutrition is Fundamental In CLD Management

Succesfull
Therapy

Th/ Complication
Antivirus

Surveilans
AntibiotiC

NUTRITION
 AntibiotiC

Antivirus

THERAPY
Surveilans SUCCESFULL

NUTRITION
Th-Complication

NUTRITION
Prevalence of Malnutrition in CLD

Malnutrition is generally found in CLD

Around 20% in decompensated condition
Up to 60% in advanced cirrhosis
Almost 100% in liver tranplantation candidate

Capocaccia L et al. J Hepatol. 1994;21{3}:317-325

Liver Function Malnutrition

Midarm circumference < 5th percentile

Triceps skin fold < 5th percentile
Alberino F et al. NutriBon. 2001
Nutrition 2001;17: 445-450

212 pasien
4 grup
1 : Malnutrisi berat
2 : Malnutrisi sedang
3 : Normal
4 : Over
Survival Based on Nutritional Status

Alberino F et al. NutriBon. 2001;17:445-450

 Nutrient metabolism in Liver Diseases
Liver function supply and inter-organ traffic of
essential nutrients (proteins, fat and
carbohydrates)
Metabolic balance disrupted in the LC
increased protein catabolism
decreased hepatic and skeletal muscle
glycogen synthesis
increased lipolysis
Bemeur C & Butterworth RF, 2014
 Alteration of metabolic status in
Chronic Liver Diseases (CLD)
Malnutrition in LC is readily understood as a
consequence of metabolic disturbances and
low spontaneous dietary intake
50% - 90% of LC patients associated with a poor
prognosis (worsening of clinical outcome,
neuropsychiatric complications, outcome
following liver transplantation)
PEM is frequently underdiagnosed in clinical
practice.
Bemeur C & Butterworth RF, 2014
Eghtesad S, etal., 2013
 Pathogenesis of malnutrition CLD
reduced nutrient intake
due to anorexia and
dietary restrictions
altered nutrient
biosynthesis
impaired intestinal
absorption
increased protein loss
Bemeur C & Butterworth RF, 2014
disturbances in
substrate utilization,
abnormalities of
carbohydrate, lipid and
protein metabolism
increased levels of pro-
inflammatory cytokines
resulting in a
hypermetabolic state
LOW DIETARY ABNORMAL
INTAKE METABOLISM
 Malnutrition related to CLD
(1) starvation-related malnutrition, which is chronic
starvation without inflammation
(2) chronic diseaserelated malnutrition, where
inflammation is chronic and of mild to moderate degree
(3) acute disease or injuryrelated malnutrition, where
inflammation is acute and severe.
Sarcopenia (loss of muscle mass) is a common complication
of cirrhosis and adversely affects survival, quality of life,
outcome after liver transplantation, and responses to stress
including infection and surgery
Obesity (BMI>30) is potential etiologic
factor for the progression to advanced liver disease
Mueller etal., A.S.P.E.N. Clinical Guidelines, 2011
 Causes of malnutrition in Advanced Liver Disease
Inadequate oral intake of
nutrient: Metabolic disturbances
(catabolism):
Anorexia
Alterations in glucose, lipid, & protein
Nausea/ emesis metabolism
Bloating/ abd distention Altered pattern of energy
Ascites consumption
Insulin resistance
Encephalopathy
Delayed gastric emptying
Malabsorption :
Restrictive diet (sodium, protein, Bile acid deficiency (cholestasis)
fluid) Small bowel bacterial overgrowth
Dysgeusia (Zn deficiency)
Alcohol intake Decreased capacity of the liver to store
Socioeconomic status nutritions
Increase in leptin
Common clinical appearence of imbalance of
nutrient:
Increased prevalence of Wernicke's
encephalopathy in LC is associated with
thiamine (vitamin B1) deficiency and
attributed to loss of liver stores of thiamine
Imbalanced in plasma levels of AAAs and
BCAAs and altered plasma and brain
BCAA/AAA ratios are implicated in the
pathogenesis of HE in cirrhosis

Bemeur C & Butterworth RF, 2014

 The Role Of BCAA
in nutritional management
of cirrhotic patients
Rasionalization of BCAA Treatment

BCAA Inhibit AAA goes through blood

brain barrier
BCAA lowering AAA plasma level
BCAA increase liver protein syntesis
BCAA reduce muscle proteolysis
BCAA could be used as energy resource
 ammonia oxidative stress cytokines

serotonine
Protein intake astrocyte
histamine Hepatic edema
Encephalopathy
GABA
BCAA
glutamine yptophan opiates
phenylalanine
tyrosine Benzodiazepines-
like
NH3
nitrogen
pool glutamate
Amino detoxification
metaboli BCAA
urea cyclic

prot
Insulin/glucagon catabolism
Liver cirrhosis
AAA breakdown
protein
synthesis

BCAA catabolism induced Hepatic Encephalopathy

General Principle
Cirrhotic Patient

Without Avoid excessive

Complication nesescity

With
Complication On demand
 Strategy of nutrition management in CLD
Clinical assessment (rescreening and reassessment)
Not at Risk

No
Yes
Continued Discharge Planning/
Admission
Inpatient Care? Continuity Care

Not at Risk
Patient Periodic
Assessment Re-screening Patient Goals Achieved
Monitoring

at Risk Change
In Status
Patient Development Implementation Patient
Screening of Nutrition of Nutrition Re-assessment Termination
Care Plan Care Plan & updating of Therapy
Of Nutrition
Care Plan

(Mueller etal., A.S.P.E.N. Clinical Guidelines, 2011)

Selected Nutrition Screening and Assessment Instrument Parameters
Instrument Screening Anthropometry and/or Diet-Related Severity of Illness Other (Px,
tools Psy Var or Symp)

Birmingham Nutrition Weight loss, BMI, appetite, ability to eat Stress factor, (severity of
Risk Score dx)
Malnutrition Screening Appetite, unintentional weight loss
Tool
Malnutrition Universal BMI, change in weight Presence of acute
Screening Tool disease
Maastricht Index % ideal body weight Alb, pre-alb, Lymp.count

Nutrition Risk Weight loss, % ideal body weight, dietary GI- function
Classification intake
Nutritional Risk Index Present and usual body weight Alb

Nutritional Risk Weight loss, BMI, food intake Diagnosis (severity)

Screening 2002
Prognostic Inflammatory Alb, pre-alb, CRP, 1-
& Nutritional Index acid glycoprotein
Prognostic Nutritional Triceps skin fold Alb, transferrin, skin
Index sensitivity
Simple Screening Tool BMI, % weight loss Albumin

Short Nutrition Recent weight history, appetite, use of

Assessment Q oral suppl or tube feeding
Selected Nutrition Screening and Assessment Instrument Parameters

Instrument Nutrition Anthropometry and/or Severity of Illness Other (Physical,

assessment tools Diet-Related Psychological Variables
or Symptoms)

Mini Nutritional Weight data, height, mid- Albumin, prealbumin, Self-perception of

Assessment arm circumference, calf cholesterol, nutrition and health
circumference, diet history, lymphocyte count status
appetite, feeding mode
Subjective Global Weight history, diet history Primary diagnosis, Physical symptoms
Assessment stress level (subcutaneous fat,
muscle wasting, ankle
edema, sacral edema,
ascites), functional
capacity, gastrointestinal
symptoms

(Mueller etal., A.S.P.E.N. Clinical Guidelines, 2011)

 Protein-energy requirements in End Stage Liver Disease
ASPEN / ESPEN
Energy requirement based on dry weight or 25 40 kcal/kg/d
determined ideal body weight if ascites is
present
ASPEN
Stable and malnourished REE x 1.2 1.4
Without encephalopathy REE x 1.2 1.4; 1.0 1.5 g/kg/d protein
Acute encephalopathy REE x 1.2 1.4; 0.6 0.8 g/kg/d protein
ESPEN
All stable cirrhosis patients 34 40 kcal/kg/d; 1.0 1.5 g/kg/d protein
Critically ill
ICU malnourished patients at risk for refeeding 15 20 kcal/kg/d ; 1.2 g/kg/d protein
ICU for maintenance caloric support 25 30 kcal/kg/d ; 1.5 g/kg/d protein
Catabolic 35 50 kcal/kg/d
Critically in obese (BMI>30) Mifflin-St Joer equoation; indirect
colorimetry for comorbidity
1.5 2.0 g/kg/d protein ideal body weight
Johnson et al. Nutr Clin Pract 2013
 General Nutritional Recommendation
For LC Patients
Nutrient Recommendation
Energy 3050 kcal/kg body weight
Sufficient to restore/maintain nutritional status and enhance
liver regeneration (adjust for obese patients)
Protein 1.01.8 g/kg body weight depending on the severity of
malnutrition (adjust if renal disease present)
Carbohydrates 4575% of caloric intake or 46 meals rich in carbohydrates
per day
Lipids 2030% of caloric intake (adjust if steatorrhea present)
Vitamins B group vitamin supplements
Particular attention to lipid-soluble vitamins
Correct specific deficiencies
Minerals Zinc, magnesium and selenium supplements
Correct specific deficiencies
Bemeur C & Butterworth RF, 2014; Silva M. etal., 2015; McClain CJ, 2016)
 Nutritional Recommendation
For LC Patients with HE
Nutrient Recommendation
Energy Optimal daily energy intake; 3040 kcal/kg body weight
Small meals evenly distributed throughout the day and late
snack of complex carbohydrates; (adjust for obese patients)
Protein Optimal daily protein intake; 1.21.5 g/kg body weight
Encourage diet rich in vegetables and dairy protein
If patient intolerant to dietary protein, consider BCAA
supplementation
Fiber 2545 g/daily
Vitamins and Multivitamin preparation in patients at increased risk of
minerals malnutrition; Correct specific deficiencies

Bemeur C & Butterworth RF, 2014; Silva M. etal., 2015; McClain CJ, 2016)
Nutritional Recommendations Related to Liver
Transplantation in Cirrhosis
The interval between listing and transplantation
(establish nutritional management before the surgical
procedure)
Prevention of further energy and nutrient depletion and
correction of macro- and micronutrient deficiencies.
Adequate calories, proteins, vitamins, minerals and trace
elements.
Determining the extent of nutritional supplementation
requires calculation of the individual patient's energy
needs

Bemeur C & Butterworth RF, 2014

Suggested Nutrition Intervention in Cirrhosis

(Krenitsky J., 2014)

 Oral intake adequate?
No Yes No

Non fungsional GI tract Non furthur intervention Diet + supplemens

Parentaral route (monitor for change status) >75% of needs
Yes No
Long term Short term Monitor for Initiates enteral feeding
> 3 weeks < 3 weeks Change status access, GI accses
obstruction?
Peripheral Central tunneld Peripheral Central No
extended catheters and standard IV standard central Inadequate
dwell port PICC catheters lines Inade
catheters Yes intake > 4-6
weeks

Nasopharingal obstruction Esophageal obstruction Gastric obstruction

Esophagostomy (rare) Gastrectomy Jejunostomy
Yes No
Gastrostomy or Nasogastric
jenunostomy
feeding
Aspiration risk? Aspiration risk?

Ye No Yes No
Postpyloric tube placement Intragastric tube placement Postpyloric Intragastric
Surgical risk? Endoscopic possible? tube tube
placement placement
Yes No
Yes No
Jenunostomi PEJ Jenunostomi Radiographic
(open or PEG Jenunostomi
(open or gastrostomy
laparascopy) laparascopy) (open or
laparascopy)
 Nutritional Route
Route Condition

Central access
TPN both long- and short-term placement
Peripheral or PPN (<2000 kcal required or <10 days)
New catheters allow longer support via this method limited to 800 to 900
mOsm/kg due to thrombophlebitis
 Advantage and disadvantage of Enteral and
Parenteral nutrition for CLD
ENTERAL PARENTERAL
Oral Nutrition Supplement increases the risk for
(ONS) is recommended for infectious complications
undernutrition patients more expensive
ONS improve nutritional Requires a greater fluid
status and survival volume
Tube Feeding (TF) improves increased incidence of
nutritional status and liver hepatic compromise (lipid
function, reduces the rate of emulsion > 1 gm/kg;
complications and prolongs carbohydrate loads)
survival. PN that provides fat, calories
TF early after liver and protein similar to a
transplantation can reduce healthy diet and EN formulas,
complication rate and cost may be the best approach
Plautha M. etal., 2006: ESPEN. Krenitsky J., 2014
 TAKE HOME MESSAGES

Malnutrition is usually found in cirrhotic

patient
Nutritional management is fundamental
volume
aside pharmacologic treatment
hepaticpredictor
Malnutrition is independent compromise (lipid
for cirrhotic patient survival
carbohydrate loads)

and protein similar to a

may be the best approach