INFECTPlE HEPATITIS

Infective hepatitis is otherwise known as viral hepatitis. This is the common cause of jaundice.
Hepatitis can be due to type A and E or due to B, C, D and G virus.

Symptoms
The symptoms of infective hepatitis are anorexia, fever, headache, rapid weight loss, loss of
muscle tone, nausea and vomiting and abdominal discomfort. The colour of urine changes from
dark yellow to red and the faeces become whitish. These develop into jaundice. The symptoms
may continue for 4-8 weeks. Neglected viral hepatitis leads to cirrhosis of liver.
Acute hepatitis B, C, D and G may lead to chronic hepatitis. Hepatitis A and E are self-
limiting.

Dietetic Managemen t
A high pr~tein, high carbohydrate and moderate fat is recommended . Small attractive meals
at regular mtervals are better tolerated. Overfeeding should be avoided.
Energy: In nasogastric feeding stage about I 000 kcals are suppli d In 1
600 to
2,000 kcals are suggested. e . severe cases '

Proteins: For the liver cells to regenerate an d ·

requirements vary accordi·ng to th . ' fa equate supply of proteins is needed. Protein
e seventy o the d · · ·1
in mild jaundice 60-80 g of protein is . d i~ease. With severe jaundice, 40 g wh1 e
permitte With he t · t ·n
containing foods are withheld as liver cannot ·b . pa ~c precoma and coma, pro ei
containing foods are recommended. meta ohse protein and only high carbohydrate
 ... .,_,,,11,111//}i'l.'i/1)/lfhl/!8,WI//JW~l/t,}l/11//l///l,Q/J\?//l//ff/l

Diet in Diseases ol' L.

'J iver and p
ancreas
Fats: Fats make the fi00 d -
and coma, due to sev . more 1
pa atable and · . . .
In severe J·a d . ere hver failure fats increase calone intake. During hepatic precoma
un ice 20 . , are not m t bO1- . . · d
·
Cases o f Jaun d. g and Ill moder t . e a ised by the hver and so fat is restncte .
ice £ t a e Jaundi 20
. ' a needs to be . ce -30 g of fat are recommended. In other
not permit fat d . · restricted 1 1·f .
igest10n and produ ~ on Y there 1s obstruction to bile flow that does
ces 1atty d · h
Ca rboh ydrates: High b •arr oea.
th t t · • car ohydrate cont · • . .
so . ~ issue proteins are not broke ent m the diet 1s essential to supply enough calones
vomttmg are present m·tr n down for energy purpose When fever nausea and
. , avenous glue . . '
feeds, mtravenous feedin h ose is suggested. As soon as the patient can take oral
· g s ould be st d . . .
given not only to provide carboh dr oppe and fruit Juices, sugar, jaggery and honey are
Vitamins· Th . y ate but also to supply adequate electrolytes.
. . . ey are essential to re .
v1tamm K and supplem t f generate hver cells. About 500 mg of vitamin C, 10 mg of
ens o B c . . .
nausea or vomiting 1·s . omp 1ex are essential to meet the daily needs. If anorexia,
present vita · · .
. , mms may be given mtramuscularly.
Mmerals: If food is not t k
and potassium lev 1 a en orally then a careful watch should be kept on the serum sodium
e s 0 ral feeds Of ~ · · ·
given orally or thr · h . iruit Juice, vegetable and meat soups with added salt are
level of sod· str
odug a n~soga ic tube, maintaining the electrolyte balance. Normal serum
mm an potassium tb · ·
mus e mamtamed through supplements.
Jntravenous feeding· It tb . ..
. · may no e possible to take oral feeds with severe nausea and vom1trng,
mtravenous administraf f . .
100 o 10 per cent glucose solut10n is recommended.

Foods Included
~~real porrid~e, soft chapathis, bread, rice, skimmed milk, tapioca, potato, yam, fruit, fruit ) J,scu;J
Jmces, sugar, Jaggery, honey, soft custards without butter cream and non-stimulant beverages.

Foods Avoided
Pulses, beans, meat, fish, chicken, egg, meat soups, sweet preparations where ghee, butter or
oil are used, bakery products, dried fruits, nuts, spices, papads, chutney, alcoholic beverages,
fried preparations, whole milk and cream.
Patients should be given enough fluid to prevent dehydration. As patients with severe hepatitis
may not be able to excrete a water load, very careful monitoring of fluid balance is necessary.
Patients tend to prefer small meals and these should be given frequently throughout the day.

CIRRHOSIS OF LIVER

Cirrhosis is a condition in which there is destruction of the liver cell due to necrosis,
fatty infiltration, fibrosis and nodular regeneration. It is a serious and irreversible disease.
Vitamin A deficiency favour the formation of cirrhosis.
The cirrhotic process may commence many years before it becomes clinically obvious and
usually the patient when first seen is at a very late stage with complications, such as ascites,
ruptured oesophageal varices or hepatic co~a. ~lmos~ 8~-90_per cent o~ liver damage also do
not produce symptoms. The initial c~ange m ~1rrhos1s IS_ widespread hver cell necrosis due
to viral hepatitis, alcohol , etc. This _ne~rosis results m_ collapse of the liver cells and
intrahepatic shunts, due to the proximity of ~he hepatic artery and portal vein to the
central vein. The necrosis and collapse also stimulate nodular regeneration and fibrosi s.
 llffllll
llifi6IIII r
LL_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ D
_ ·~
ie~

Cirrhosi s of liver is the structural and functional end result of nutritional, infecti ve or
toxic changes in the liver.

Aetiolog y
Viral infection: The hepatitis viruses B, C, D and Gare more likely to Produce cirrhosis.
Alcohol : It has a direct toxic effect on the liver. It occurs after years of excessive alcohol
intake in individuals whose diets are less than optimal in a number of nutrients. It i~ eS timated
that 60 g alcohol for men and 20 g for women taken daily over a _prolong_ed penod of time
increases the risk of cirrhosis. A chronic alcoholic is often deficient 1Il protems, ~arbohydrates
and vitamins. These make the liver highly vulnerable to any infection or tox~n. Alcohol is
also known to have direct action on the lipid metabolism in liver by ~ 1) e~ancmg _fatty acid
synthesis; (2) decreasing fatty acid oxidation; (3) producing specific stimulatwn to tnglyceride
formation leading to fatty liver; (4) decreased release of lipoproteins and (5) enhanced uptake
of circulating lipids. .. . .
Alcohol can cause 'deadly ' damage to the liver. It enhances B and C hepatitlc mfect1ons
and exacerbates drug toxicity.

Healthy Liver Cirrhotic Liver

Fig. 18.3 Normal liver in comparison to liver in alcoholic cirrhosis, showing the characteristic diffuse
nodularity induced by the underlying fibrous scarring

Nutrition: Malnutrition aggravates any injury to the liver particularly vitamin A, ~-carotene
and vitamins E anJ...-£. n _J , ---=-
~ -- - " ~o cJ , o.nUt
Toxins of food: Aflatoxin may be one of the causes of cirrhosis. Chillies and spices are irritant
foods which when absorbed are likely to damage the liver cells. However, the effect of such
substances on the liver is as yet unknown. Metabolic disturbances such as haemochromatosis (no
control on iron absorption) or Wilson's disease (disturbance in copper metabolism) can lead to
cirrhosis of liver.
Indian childhood cirrhosis is a common disease in India. The clinical and histological features
are similar to those of adult cirrhosis. Usually they are seen between the age of 1 to 3 years
but even babies less than a year old may show an advanced stage of the disease.

Symptoms and Clinical Findings

The onset of cirrhosis may be gradual with gastrointestinal disturbances such as anorexia,
nausea, vomiting, pain and distension. The patient may also suffer from weakness, muscle
 l L1,cl i11 Diseascs- ;;i-L.
- - - 2 zver and p

occu~
.
cramps, We ight Ioss and ~
ancreas
1 ever A
· s the ct·
~-----------m ,
Ascite · th isease progr .
s IS e accUJnul f esses Jaundice and other serious changes
as a consequence of 10
a n of abno
11 0 .d po~ 1 v . nna1 amount
~o ~ osmotic pressur u ein h!'Pertension, obst s 0 _f fluid in the ab~om~n. It ma~ develop
1mparred water excretion~ > to unpaired albu . ruction o~ th~ hepatic vem,(Jf fall m p_lasma
Oesophageal van·c nun synthesis, rncreased sodium retent10n or
es or va.
deve lop as a complicatio ncose Veins in the oe
and may be provoked b n of Portal hyPertension sophagus and ~pper part of the stomach may
The haemorrh . Y roughage of any ki · Haemorrhage 1s then an ever present danger
. age itself ma nd.
ammorna and subse Y be fatal or th bl . .
patients. quent hepatic coma G e ood may provide for the accumulat10n of
· reater prevalence of PEM is found in alcoholic
Principles of Diet
A high calorie, high prot . h.
·
l1e lps lil . em, igh carboh dr
regeneration of liv Y ate, moderate or restricted fat high vitamin diet
. er and helps t0 '
supp 1ementat10n of fat sol bl . . prevent the formation of ascites. Low fat with
. d
restncte only when there •u e v1tamms
.
a11d . l .
mmera s should be given. .
Sodmm should be
. 1s asc1tes.
Fibre should be restricted wh .
hypertension. The diet sh ld b en t~ere Is danger of oesophageal varices and portal
ou e attractive and palatable.
Dietary Treatment
Energy: Consumption of food IS
· d'ffi
• . 1 cu 1t because of anorexia
· and asc1tes.
· ·
The patients are
usually
. . emaciated
. by. the tun· e cITT
· h os1s· of the 1·1ver 1s
· d.1agnosed. The patient
· · ·
requues highly
nutnt10us food 1.e., high calorie diet is necessary because of prolonged undernourishment. The
calorie requirement should be between 2000- 2500 kcals.
Proteins: The serum albumin which is exclusively synthesised by the liver cells, is low in
cirrhosis and aggravated by the loss of a considerable amount of albumin into ascitic fluid. A
high protein diet is helpful for regeneration of the liver. In the absence of hepatic coma a high
intake of proteins about 1.2 g/kg of body weight can be given. If the patient is in precoma or
coma, proteins should be withheiatill the patient tides over the crisis. In cirrhosis there is rapid
breakdown of liver cells. The protein content of the diet varies according to the symptoms. The
increased amounts of proteins can be met by the addition of casein _(milk pr~t~in concentr~te)
which can be added in milk, soups and ice creams. Vegetable protems contammg more valme
is beneficial in preventing encephalopathy.
· ·ven Even if fatty changes are present in the liver, fats should be
F ats: Ab out 20 g o f f:a t 1s g1 . . . . . . . .
· • t of protein is supplied. Medmm cham tnglycendes contallllllg
given provided adequate amoun s · h
. b · as these are digested and absorbed m t e ab sence o f b'l ie
C to C fatty acids can e given .
s}lts. C~~onut oil contains medium chain fatty acids. . . ~
r d liberally so that the liver may store glycogen. Liver ~
Carbohydrates: Should be supp ie t of glycogen is present in liver cells. ~ixty per cent ~
fu . .
nction improves w
hen an adequate s ore . . . . d
b h drate so that liver damage 1s mm1m1se .
t
<
. h Id come from car o y ~
o f th e ca1ones s ou . . ma·or site of storage and conversion of vitamins ~
. M. ls. The hver is the J . f ti 1 .b
V1tamins and mera · . hosis the liver concentrat10n o o ate, n ofl avm,
. U
into their metabolically active form. In cirr '
 Dietetic! ]
Il l E decreased
A are decreased which may be due to
nico tina mid e, vitamin B and vitamin the liver,
hesi s of retin ol bindi'~g prot ein. Sinc e vitamin o is converted to calcidiol in
synt in raising
D in biliary cirrhosis is not successful
oral adm inis trati on or injection of vitamin B vitamins is required to
th e seru m level of calcidiol. Vitamin supplementation especially of
Sodium is
are useful if fatty infiltration is present.
prev ent anaemia. Choline and methionine
rest ricte d in oed ema and ascites. icted to
ary sodium intake may initiall~ be restr
In all patients with cirrhotic ascites diet
ml/d ay) is reqm red for patients
4 00-800 mg/ day. Restriction of fluid intake (800-1000 salt is
with hyp ona trem ia (serum sodium <
125 mEq/1). If there is no ascites very little
.for ascites
itted to mak e the food mor e appe tising. Pota ssiu m salt is ad!n inis~ered
perm ents hence
Anaemia is com mon amo ng cirrh osis pati
and oed ema to prev ent hypokalaemia. afte r mea~s
s sulphate ~ s daily
iron supp lem enta tion is essential.'~ rrou macrocyhc
orally is indicated m the trea tme nt of
should_ be giveEJ Folic acid 1 mg/ d
ana emi a. feeding
ke by eating, supp lem enta tion with sip
If pati ent cann ot maintain a sufficient inta considered.
te, enteral supp lem enta tion shou ld be
sho uld be con side red. If this is inadequa unsuccessful
for patients in who m enteral nutr ition is
Pare nter al nutr ition should be reserved n of ascites
to risk of catheter sepsis and poo r reso lutio
and to be give n only for short time. Due
of feeding.
pare nter al nutrition is not the best choice and
and maintenance of adeq uate calorie, fluid
Hep atic herb al supportives, antioxidants
inely recommended.
elec troly tes, fat soluble vitamins are rout

HEPATIC ENCEPHALOPATHY
elop as a
neurologic dist urba nces whi ch may dev
Com plex synd rom e char acte rise d by n containing
results from entr ance of cert ain nitr oge
com plic atio n of severe liver disease. It d by the
bral circulation with out bein g met abo lise
subs tanc es such as amm onia into the cere ion in
be a cons eque nce of shun ting of the portal bloo d into the syst emi c circulat
live r. It may
in hepatitis.
cirrh osis or of severe damage to liver cells
I
I

/' r, ,IJ' 1~·~ •• '

J,' .• , ' _-_j/
Precipitatory factors l)I •))'-"; ,._,, ' I .
ary protein
ns, surgical proc edu res and exce ssiv e diet
Gastrointestinal bleeding, severe infectio nylalanine
a. Plas ma aromatic ami no acid levels, (phe
and sedatives may precipitate hepatic com ine, leucine
while branched-chain ami no acids (isoleuc
and tyrosine) and methionine are elevated pattern
ed that alterations in the plas ma ami no acid
and valine) are lowered . It has been postulat
may be usua lly related to encephalopathy.

Sym pto ms
sine ss are
prop riate beh avio ur, deli rium and drow
Con fusi on, restlessness, irritability, inap n extended .
ent. The re may be inco ordi nati on and a flapping trem or of the arms and legs whe
pres . The breath
may go into com a and hav e con vuls ions
Elec troly te imb alan ce occurs. The pati ent
imp erat ive or deat h occurs.
has a faecal odour. Prom pt treatment is

Treatment
formation
i~ emp erlc al and base d on prev enti ng the
The treatm~nt of hepa tic ~ncepha~opat~y
pally amm onia .
and absorption of gut- den ved toxms/prmc1
 ro,~I in Diseases of Liver and p ancreas J- ,
The prevalence of protein
. . energy maln tr· . . . . d.
to seven ty of hepatic damage. u ition m patients with liver disease vanes accor mg
Factors that contribute to ..
. . 1
excessive protem losses impa· ma d nutrition
. .
are poor dietary . •
mtake nutrient ma la b sorp t'1on
' Ire prote . '
Efforts should be made to ma. . In synthesis and difficulty in utilization of fuel sourc~.
liver disease. Patients with more mtam no_nnal dietary intake in patients with stable chr?mc
and nutritional supplemen tatio severe hver dysfunction will require dietary modificati ons
n.
Calo ric in~akc: During the first to _ _ . . . .
or JV infus10n of I 00 per ce t d.24 4 ~ houis of adm1ss10n with encephalopathy mtra gastnc
of energy. Most patients im n 1xtrose . m water can be given. - The goal 1•s to prov1·d e a source
prove
They can resume oral diet h . h with Iactul d · · · · · · · Dg caus e
. ose an with ehmmat10n of prec1p1tat1 ·
. . . _w Ic contams 30-40 kcal/kg/d.
Protcm mtakc. A low sodmm iso
protein hydrolysa tes and d. mo 1_a r f~rmula _containing glucose, polymers, casein or_ soya
Standard amino acids can~ee ~um cham tng_lyc~ndes is well tolerated by critically ill_pat1e~ts.
f . .d . sed. Nom1ahzation of the ratio of branched chain ammo acids
to aro~a IC a_m i~o aci s improves encephalopathy, nutritional status and short term survival.
Daily protien
. mtakes
. . in pat'ien ts wit· h CIIThos1s
· · should be 1.0 · · .•
to 1.5 g/kg. Protein !'es-ffi0t'l'tffl
should. . be av01ded m patients with h · . · ·
. . . epatic encephalopathy. Some patients may require a transient
re str~ctto~ of daily protem mtake to 0.5 g/kg. In protein intolerant patient, nitrogen should be
provided m the fonn of an amino acid supplement.
Fuel utilisation and nitrogen economy are optimised in these patients by provision of four to
seven small meals. A late-night snack of complex carbohydrate should be given. The feeding
pattern should ensure even distributio n of protein throughout the day thereby avoiding protein
loading.
Dairy protein and vegetable proteins are better tolerated. The increased tolerance to vegetable
protein diets reflects their high dietary fibre content. Fibre effects on colonic function, namely
decreased transit time, increased intraluminal pH, stimulation of microbial growth and increased
faecal ammonia excretion. Plama arginine and citrulline concentrat ions tend to be higher in
patients on vegetable protein diets. This may facilitate ammonia removal via the Krebs-Hen seleit
cycle.
In general, patients should be encourage d to take 30-40 g of vegetable protein. Branched
chain amino acids can be given to malnouris hed decompen sated cirrhotic patients w ith hepatic
encephalo pathy who are intolerant of dietary protein.

Dietary Guidelin es
A wholesom e well-bala nced diet maintains the health of liver and minimise further damage.
It can also help immune system and fight off illness.
• A healthy calorie intake should be maintaine d.
• Vegetable and dairy proteins are preferred.
• If needed dietary suppleme nts containing certain types of amino acids can be included.
• Diet should include whole grains at least five servings of fruits and vegetable s of varying
colours.
• Salt, sugar and fatty foods should be restricted.
•fJ•/ - - - 1I
._______- - " ' - - - - - - - - - - - - - - - - - - - - - - - - - - Dietetics
• A minimum of 6-8 glasses of fluids per day should be taken. In addition to water, juices,
tea, milk and soups can be taken.
• Small and frequent meals should be taken and long periods of fasting is avoided.