Nutritional Management of

Liver diseases
By
Yasmin Saad
Professor of Hepatogastroenterology
Cairo University
Consultant of Clinical Nutrition, 57357 CCHE
NNI Diploma & ESPEN Certified
Introduction

Anatomy & Position

Functions of liver

Causes of liver diseases

Assessment of liver severity

Malnutrition in liver diseases

Energy Requirements, Macro & Micronutrients in CLD

Specific considerations

Enteral nutrition in CLD

PN in CLD & its complications

 Introduction
The liver is one of the main organs of nutritional metabolism, including
protein synthesis, glycogen storage, and detoxification.

Liver functions become damaged to a greater or lesser extent in patients

with liver diseases, resulting in various metabolic disorders, and their
disturbed nutritional condition is associated with disease progression.

Dietary counseling and nutritional intervention can support other medical

treatments in some liver diseases.
Liver Anatomy & Position
Causes of liver disease according to
onset
Pathophysiology of liver disease
Classification of LC
Severity of liver disease
Malnutrition in liver disease
 Prevalence of malnutrition
In LC, the prevalence and severity of PEM are related to the clinical stage of chronic liver
disease:

o 20% in well compensated disease

o >60% in advanced cirrhosis

Etiology of liver disease per se does not influence the prevalence and degree of malnutrition and
protein depletion

Higher prevalence & more degree of malnutrition in alcoholics due to (unhealthy life style and
socio-economic deprivation).
 Patients with ESLD present with:

 Muscle wasting

 Decreased fat stores

 Fat-soluble vitamin deficiencies

 Anemia from (iron, folate, and pyridoxine deficiency)

 Altered cell-mediated immune function

 Nutritional Screening &
Assessment in Liver patient
 Screening of malnutrition

 Liver disease patients should be screened for malnutrition using a validated

tool

 NRS-2002 and MUST are validated tools to screen hospitalized patients

for risk of malnutrition & are recommended by ESPEN.
MUST
 New developing tool

RFH-NPT has been developed as a screening tool for malnutrition in

liver disease patients

None of the available screening tools has been validated rigorously in

LC patients leaving RFH-NPT as the best option currently available

ESPEN, 2018
 Bedside Tools for Nutritional
Assessment

The accurate quantitative measurement of nutritional status is difficult in

chronic liver disease patients with fluid overload and/or impaired hepatic
protein synthesis (e.g. albumin)

In LC, nutritional status can be assessed using bedside methods e.g. SGA

MAC and TSF are non-invasive bed-side methods but suffer from high
inter-observer variability.
Anthropometric Measures
 Bedside tools for nutritional assessment

The modified (RFH-SGA) combining SGA and anthropometry.

 The RFH-SGA is a strong predictor of morbidity and mortality, but it is time

consuming and requires a trained dietician.

Handgrip strength is lower in protein depleted LC patients & a good predictor of

the rate of complications within the next year.

Handgrip strength is better preserved in LC of viral otherthan alcoholic or

cholestatic etiology.
 Sarcopenia
 Sarcopenia is the key feature of malnutrition in LC patients

 Assessed by radiologic methods (DXA, CT) to detect loss of muscle

mass or by tests of muscle function such as exercise test or 6-min walk
distance.

 In NASH, cirrhosis and LT, the presence or absence of sarcopenia

should be assessed since sarcopenia is a strong predictor of mortality
and morbidity
 ESPEN 2018

Phase angle (measured by bioelectrical impedance analysis) or

handgrip strength allow assessment of mortality risk

Radiologic methods (DXA or when CT/MRT images are available for

other reasons) should be used to diagnose sarcopenia
Nutritional intervention in ALF
 Malnutrition in ALF
ALF typically affects young adults and develops in the absence of pre-

existing chronic liver disease.

Its rapidity of development is such that most patients will not have

evidence of malnutrition at time of illness onset, though nutritional

compromise may develop during the period of acute illness severity,

resolution and recovery.

Types of ALF
 Nutrition in different types of ALF
In ‘hyper-acute’ liver failure: due to the short duration of illness in most patients
nutrition support is thought to play a relatively minor role.

In the other subtypes of ALF early nutrition support is more often necessary.

There are no data on the optimal methods to assess nutritional status in patients
with ALF. It seems that simple bedside tools such as SGA or anthropometry are
adequate for identifying patients with malnutrition
 When is nutritional therapy indicated to support recovery
from ALF?

In malnourished ALF patients enteral nutrition (EN) and/or parenteral

nutrition (PN) should be initiated promptly, as in other critically ill patients.

ALF patients without malnutrition should be provided with nutritional

support (preferentially EN) when they are considered unlikely to resume
normal oral nutrition within the next five to seven days, as in other critical
Illness
 When is nutritional therapy contraindicated to
support recovery from ALF? (Cont.)

In patients with severe hyper-acute disease with hepatic encephalopathy and

highly elevated arterial ammonia who are at risk of cerebral edema, nutritional

protein support can be deferred for 24-48 h until hyper-ammonemia is controlled.

When protein administration is commenced, arterial ammonia should be

monitored to ensure no pathological elevation occurs

 Which are the conditions to safely use oral
nutrition to achieve adequate nutrient supply?

Patients suffering from only mild HE can be fed orally as long as

cough and swallow reflexes are intact.

In patients with mild HE oral nutritional supplements (ONS) should

be used when feeding goals cannot be attained by oral nutrition alone.

 Who cannot be fed orally in ALF?
According to ESICM guidelines, low dose EN should be started when acute,
immediately life-threatening metabolic derangements are controlled with or
without liver support strategies, independent on grade of encephalopathy

PN should be used as second line treatment in patients who cannot be fed
adequately by oral and/or EN

Standard enteral formulas can be given, as there are no data regarding the
value of a disease specific composition
 Chronic Liver Disease

Metabolic (NAFLD/ NASH)

Liver cirrhosis (compensated, decompensated)

NAFLD/NASH
Liver cirrhosis (LC)
 Hepatic decompensation
Acute decompensation: acute liver cell failure (fulminant)
Chronic decompensation: part of natural history or may be precipitated by
GI bleeding
Hypotension
Hepatotoxic Drugs
Infection
HCC
General Anesthesia
Surgery
Why? Reduce cardiac output, induce splanchnic VD, reduce hepatic blood flow (30-50%)
 Nutritional Management of LC

Multidisciplinary nutrition care should include monitoring of

nutritional status and provide guidance for achieving nutritional goals

& improve patients' long-term outcome/survival.

EASL, 2019
 Energy Expenditure

Cirrhotic patients in conditions of increased energy expenditure (i. e.

acute complications, refractory ascites) or malnutrition, should ingest an

increased amount of energy

In cirrhotic patients, an increased energy intake is not recommended in

overweight or obese patients

 Energy Expenditure

 In patients with significant ascites, base calorie needs on an estimated

"euvolemic" weight (ABW) to prevent overfeeding

 Refeeding Syndrome
Occur in patients who have adapted to starvation and then receive increased

calories (especially carbohydrate).

The increased calorie provision results in increased endogenous insulin production

Decrease (at times dramatic) in serum potassium, magnesium, and phosphorus as

these ions move from the intravascular, into the intracellular space.

Refeeding syndrome is also associated with increased cardiac and respiratory rate,

as well as fluid and sodium retention.

 Oral Diet
 Periods of starvation should be kept short by consuming three to five

meals a day and a late evening snack should be recommended to

improve total body protein status.

 Protein Requirements

Non-malnourished patients with compensated cirrhosis should ingest

1.2 g/kg/d protein

To replenish malnourished and/or sarcopenic cirrhotic patients the

amount of 1.5 g/kg/d protein should be ingested

 Protein Type in HE

Protein intake should not be restricted in cirrhotic patients with HE as it

increases protein catabolism

Early reports of benefits of BCAA enriched formulas to improve

encephalopathy
 Protein Type in HE

In cirrhotic patients who are protein “intolerant”, vegetable proteins or BCAA

(0.25 g/ kg/d) should be used by oral route to facilitate adequate protein intake.

Long-term oral BCAA supplements (0.25 g/kg/d) should be prescribed in patients

with advanced cirrhosis in order to improve event-free survival or quality of life

 Micronutrients
 Patients with LCF are at increased risk of deficiencies of several micronutrients

 Patients with ongoing alcohol ingestion are at further increased risk of thiamine,

magnesium and folate deficiency

 Patients with cholestatic liver disease and those with a suspicion of fat

malabsorption should have levels of vitamin A, 25-hydroxy vitamin D and

Vitamin E checked at baseline, and rechecked each year

 Micronutrients
 Zinc deficiency is common in patients with cirrhosis due to:

 Decreased dietary intake of meats

 Increased urinary excretion due to diuretic use
 Increased zinc needs

 Zinc is essential for the function of over 300 enzymes, including those of the urea cycle.

 Some reports have suggested that supplemental zinc may improve encephalopathy scores
 Recent RT failed to document a significant improvement of encephalopathy scores despite
a normalization of serum zinc levels
General consideration of nutritional
intervention in liver disease
 LC
In patients with cirrhosis, a high prevalence of malnutrition, protein
depletion and trace element deficiency should be anticipated.

In LC, a stage dependent progressive impairment of carbohydrate,

protein and lipid metabolism characterized by hepatic glycogen
depletion, impaired non-oxidative glucose metabolism and reduced
albumin synthetic rate should be anticipated
 ALF

In acute liver failure (ALF), due to subtotal loss of hepatocellular function
and ensuing multi-organ failure, a severe derangement of carbohydrate,
protein and lipid metabolism should be anticipated characterized by
impaired hepatic glucose production and lactate clearance as well as protein
catabolism associated with hyper-aminoacidemia and hyper-ammonemia
 LTx
After LTx for LC, prolonged incomplete recovery of total body nitrogen
status should be anticipated

After LTx, the risk of developing sarcopenic obesity and metabolic

syndrome should be taken into account and nutritional rehabilitation
should aim for an earlier and faster recovery of total body protein and
muscle function
 REE
In ALF, ASH and cirrhosis, REE is usually increased.

Patients with NAFLD have a normal REE.

Due to considerable inter-individual variability, REE should be

measured using indirect calorimetry, if available.

Patients with chronic liver disease and a sedentary lifestyle should

receive a total energy supply of 1.3 x REE.
 Ascites
 Dietary treatment for ascites includes sodium restriction in addition to diuretic
therapy.
 Sodium is commonly restricted to 2 g/day.
 Caution is warranted because of limited palatability and the risk of over
restricting sodium.
 Adequate protein intake is also important when a patient undergoes frequent
paracentesis
Sources of Dietary Sodium
 Hyponatremia

 Fluid intake is usually restricted to 1 to 1.5 L/day, depending on the

severity of the edema and ascites.

 A moderate sodium intake should be continued because excessive

sodium intake will worsen fluid retention and the dilution of serum
sodium levels.
 Probiotics & HE

It has been proposed that probiotics and synbiotics (sources of gut-friendly
bacteria and fermentable fibers) can be used to treat hepatic encephalopathy.

Probiotics may improve hepatic encephalopathy by reducing ammonia portal

blood or by preventing production or uptake of lipopolysaccharides in the gut.

Thus they decrease inflammation and oxidative stress in the hepatocyte (thus
increasing hepatic clearance of toxins including ammonia), and minimizing
uptake of other toxins.
 Glucose Alterations
Glucose intolerance occurs in almost two thirds of patients with cirrhosis, and
10% to 37% of patients develop overt diabetes (IR in peripheral tissues)

Hyperinsulinism also occurs in patients with cirrhosis, possibly because

insulin production is increased, hepatic clearance is decreased, portal systemic
shunting occurs, there is a defect in the insulin-binding action at the receptor
site, or there is a post-receptor defect.
 Fasting hypoglycemia
Low blood glucose can occur because of the decreased availability of glucose from
glycogen in addition to the failing gluconeogenic capacity of the liver when the patient has
ESLD.

Hypoglycemia occurs more often in acute or fulminant liver failure than in chronic liver
disease.

Hypoglycemia may also occur after alcohol consumption in patients whose glycogen stores
are depleted by starvation because of the block of hepatic gluconeogenesis by ethanol.

Nutrition therapy involves balanced meals with small, frequent snacks to avoid periods of
fasting.
 Fat Malabsorption

 Due to decreased bile salt secretion (as in PBC, sclerosing

cholangitis, and biliary strictures), administration of neomycin or
cholestyramine, and pancreatic enzyme insufficiency

 Dietary fat with medium chain triglycerides (MCTs) may be useful.

 Because MCTs do not require bile salts and micelle formation for
absorption, they are readily taken up via the portal route
 Hepatorenal Syndrome

 It is renal failure associated with severe liver disease without intrinsic

kidney abnormalities.

 Diagnosis: when the urine sodium level is less than 10 mEq/L and
oliguria persists in the absence of intravascular volume depletion.
 Hepatorenal Syndrome
 Treatment:

Conservative therapies, including discontinuation of nephrotoxic drugs,

optimization of intravascular volume status, treatment of underlying infection, and
monitoring of fluid intake and output.

If fails dialysis may be required.

In any case, renal insufficiency and failure may necessitate alteration in fluid,
sodium, potassium, and phosphorus intake
 Osteopenia
 often exists in patients with PBC, sclerosing cholangitis, ALD,
hemochromatosis & in patients who have had long-term treatment
with corticosteroids.

 Corticosteroids increase bone resorption; suppress osteoblastic

function; and affect sex hormone secretion, intestinal absorption of
dietary calcium, renal excretion of calcium and phosphorus, and the
vitamin D system.
 MNT
 Weight maintenance

 Ingestion of a well-balanced diet

 Adequate protein to maintain muscle mass

 1500 mg of calcium per day

 Adequate vitamin D from the diet or supplements

 Avoidance of alcohol

 Monitoring for steatorrhea, with diet adjustments as needed to minimize

nutrient losses.
Diagnosis and management of bone disease
in patients with chronic liver disease
 Enteral Nutrition
In cirrhotic patients, who cannot be fed orally or who do not reach the nutritional

target through the oral diet, EN should be performed

Esophageal varices are no absolute contraindication for positioning a nasogastric

tube

PEG placement is associated with a higher risk of complications, due to ascites or

varices, and thus, can only be used in exceptional cases

 Parenteral Nutrition

 Parenteral nutrition is associated with increased infectious and metabolic

complications compared to enteral feeding.

 Parenteral nutrition should be reserved only for those patients who cannot receive

enteral nutrients, (ileus, small bowel obstruction, etc.).

 Peripheral parenteral nutrition has limited utility, due to the increased fluid volume

required to provide significant calories and protein.

 Parenteral Nutrition

 The optimal composition of macronutrients in TPN for patients with hepatic

failure is unclear.
 TPN that provides either excessive lipid or dextrose has been implicated in
exacerbating hepatic compromise.
 When parenteral nutrition is required, it is recommended to limit IV lipid
provision to less than one gram of long chain fat per kg and providing a balanced
fuel source
Nutrition associated liver injury
 In Children

Severe malnutrition in children can cause fatty liver which in general

is fully reversible upon refeeding

In infants and children, PN can cause cholestasis, therefore named

parenteral nutrition-associated cholestasis (PNAC)

 In Adults (IFALD & PNALD)

 Incidence of advanced IFALD/PNALD ranges from 0 to 50 % and

mortality ranges from 0 to 22 %.

 Progressive IFALD/PNALD is an accepted indication for a timely

lifesaving small bowel transplantation
 In Adults (IFALD & PNALD)

 IFALD/PNALD is related to female gender, age, length of time on

PN, total caloric intake, and lipid or glucose overload

It is difficult to differentiate between the role of the underlying

condition (extensive small bowel resection, sepsis) and that of PN in
the pathogenesis of PNALD
 In Adults (IFALD & PNALD)

In adults, less data is available regarding the effect of modifying

quantity and/or composition of parenteral lipid on the course of

PNALD.

Limiting soy-bean based lipid to <1.0 g/kg/d has been suggested

lipid emulsions with a reduced n6/n3 ratio can be used

Impact of Nutrition on prognosis in liver
disease
 Impact of Nutrition on prognosis in liver disease

In ALF patients, obesity is associated with an increased risk of death or need
for Tx and an increased mortality after Tx.

In the management of severely malnourished ASH and cirrhosis patients, a

poorer survival compared to non-malnourished patients shall be expected

In assessing the prognosis of patients in whom NAFL/NASH is an integral

component of the metabolic syndrome the effect of non-hepatic comorbidity
should be considered.
 Take home messages
Full feeding in the acute phases of critical illness does not provide an
advantage over trophic feeding and may be harmful

 Nutrition prescriptions should be tailored for pre-admission nutrition

status, and severity and stage of illness.

 Aim to meet energy and protein requirements by EN first

Advise regular meals and snacks

 Take home messages

 Advise a late evening 50g carbohydrate snack

 Nutritional supplements are often needed - try milk based ones first
 Calcium and vitamin D supplementation is advised for bone health
 Thiamine and vitamin B supplements are advised for patients with a
history of hazardous or dependent drinking