This case presentation summarizes the hospital admission of a 35-year-old male diagnosed with Grade II alcoholic liver disease and hepatic encephalopathy. He presented with fever, swelling of the feet and knees, loss of appetite, and sleep issues. His medical history revealed chronic alcohol use and tobacco chewing. On examination, he exhibited pallor, edema, and jaundice. Laboratory tests showed elevated liver enzymes. He was diagnosed with Grade II alcoholic liver disease and hepatic encephalopathy based on his symptoms, risk factors, and diagnostic tests. He was treated medically and counseled on lifestyle modifications and medication adherence.

1. 1
Presented by:
K. Prathyusha
12352D.1009
Pharm.D V yr.
Under the Guidance of
Dr. J. Sandeep Reddy
MD,DNB Gastroenterology
MGM HOSPITAL
Department of Pharmacy Practice
CARE COLLEGE OF PHARMACY
OGLAPUR, ATMAKUR, Warangal – 506311, (T.G) India.
CLERK SHIP-II
DEPARTMENT OF GASTROENTEROLOGY
Academic year 2015-2016

2. CASE PRESENTATION
A 35 year old male was admitted in the acute medical ward on 06/04/2016.
Patient came with the complaints of fever since 3 months, swellings of both
feet since 10days gradually progressed to knee, loss of appetite and sleep
since 1wk. Patient was apparently asymptomatic 3months ago then he
developed high grade fever with chills, intermittent subsides with
medications and relapses. He is a Chronic alcoholic – gudumba 1lit/day since
6yrs, non-smoker having a habit of tobacco chewing since 15 yrs. Bowel and
bladder movements are regular.
2

3. SUBJECTIVE
Name: MS Age/sex: 35y/M IP#:12335
Ward: AMW/M2 DOA: 6/4/16 DOD: 11/4/16
Reasons for admission: Patient came with the complaints of fever since 3
months, swellings of both feet since 10days gradually progressed to knee, loss
of appetite and sleep since 1wk.
History of present illness: Apparently asymptomatic 3months ago then he
developed high grade fever with chills, intermittent subsides with
medications and relapses.
Past medical history: Insignificant
Family history: Insignificant.
Personal history and habits: Chronic alcoholic – gudumba 1lit/day since 6yrs,
non-smoker having a habit of tobacco chewing since 15 yrs. Bowel and
bladder movements regular 3

4. OBJECTIVE
Physical examination Systemic examination
Blood Pressure: 100/60mmHg CVS: S1+S2+
Temperature: 360 CNS:
PULSE: 94bpm RS: clear
Respiratory Rate: P/A: Distended & Tender
4
General examination: Pallor, B/L Pedal edema [Pitting type], Icterus
Radiological examination: ----

5. LABORATORY DATA
5
Parameter Report Normal value
RBS 60 70 – 130mg / Dl
Urea 52 10 – 40
Sodium 135 135 – 145 mmol/l
Potassium 4.1 3.5 – 5.5 mmol/l
S.Cr 2mg/dl 0.9-1.6
SGPT 185.5 0 – 35 U / L
SGOT 61 36 – 141 KA Units
Bilirubin:
Total
Direct:
2.4
1.11
0.2 – 1 mgs %
0 – 0.2
Cl 119 98 – 99 mmol/l

6. HEPATIC ENCEPHALOPATHY WITH ALD:
Alcohol’s harmful effects on liver cells not only interfere with the
normal functioning of the liver but also impact distant organs, including the
brain. Prolonged liver dysfunction resulting from excessive alcohol
consumption can lead to the development of a serious and potentially fatal
brain disorder known as hepatic encephalopathy (HE).
It is a brain dysfunction caused by liver insufficiency and/or PSS; it
manifests as a wide spectrum of neurological or psychiatric abnormalities
ranging from subclinical alterations to coma.
The most commonly used staging scale of HE is called the West Haven
Grading system:
 Grade 0: Minimal HE-Asymptomatic, coordination impairment, poor
thinking ability.
 Grade 1: Mild HE-Mood changes like depression/ irritability and have
sleep problems
 Grade 2: Moderate HE- Inappropriate behavior, slurred speech,
impairment in mental status, difficult writing.
 Grade 3: Severe HE- Drowsiness, unable to perform mental tasks, strange
behavior, extremely anxious.
 Grade 4: Coma-Unconscious and slips into coma.
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7. SYMPTOMS
Symptoms of hepatic encephalopathy differ depending on the underlying
cause of the liver damage.
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Moderate Severe
Difficulty thinking
Personality changes
Poor concentration
Problems with handwriting or loss of other small-hand
movements
Confusion
Forgetfulness
Poor judgment
A musty or sweet breath odor
Confusion
Drowsiness or lethargy
Anxiety
Seizures
Severe personality changes
Fatigue
Confused speech
Shaky hands
Slow movements

8. CAUSES:
 Infections
 Kidney problems
 Dehydration
 Low oxygen levels (hypoxia)
 Recent surgery or trauma
 Use of medications to suppress the immune system
 Eating too much protein
 Use of medications (such as barbiturates or benzodiazepine tranquilizers)
that suppress the central nervous system
 Electrolyte imbalance, especially a decrease in potassium after vomiting or
taking diuretics
 Alcohol
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9. PATHOPHYSIOLOGY:
9

10. DIAGNOSIS:
 The diagnosis of hepatic encephalopathy can only be made in the presence of
confirmed liver disease (types A and C) or a portosystemic shunt (type B), as its
symptoms are similar to those encountered in other encephalopathies.
 To make the distinction, sodium, potassium, ammonia, abnormal liver function
tests and/or ultrasound suggesting liver disease are required, and ideally liver
biopsy.
 The symptoms of hepatic encephalopathy may also arise from other conditions,
such as cerebral haemorrhage and seizures (both of which are more common
in chronic liver disease).
 A CT scan of the brain may be required to exclude haemorrhage, and if seizure
activity is suspected an electroencephalograph (EEG) study may be performed.
 Rarer mimics of encephalopathy are meningitis, encephalitis, Wilson's disease;
these may be suspected on clinical grounds and confirmed with investigations
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11. TREATMENT:
 The treatment of hepatic encephalopathy depends on the suspected underlying
cause (types A, B or C) and the presence or absence of underlying causes.
 If encephalopathy develops in acute liver failure (type A), even in a mild form
(grade 1–2), it indicates that a liver transplant may be required.
 Hepatic encephalopathy type B may arise in those who have undergone a TIPSS
procedure; in most cases this resolves spontaneously or with the medical
treatments, but in a small proportion of about 5%, occlusion of the shunt is
required to address the symptoms.
 In hepatic encephalopathy type C, the identification and treatment of
alternative or underlying causes is central to the initial management.
 Given the frequency of infection as the underlying cause, antibiotics are often
administered empirically (without knowledge of the exact source and nature of
the infection). Once an episode of encephalopathy has been effectively treated,
a decision may need to be made on whether to prepare for a liver
transplantation or not.
 Medications mainly used are lactulose, l-ornithine and l-aspartate, flumazenil.
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12. PRESCRIPTION DRUGS
Drug Category Use Toxicity monitoring
parameters
Dose
Lactulose Laxative helps in
elimination of
ammonia
Hypernatremia,
GI upset, excessive
sweet taste
10g/15
ml
Lactitol Laxative Prevents
thrombosis
Hypernatremia
Neomycin Macrolide Prevents
bacterial
growth
Nephro-ototoxicity 500mg
Rifaximin Antitubercular
agent
Bacterial growth
inhibition
Neurotoxicity 200mg
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Neomycin-2-4g/d, Paromomycin-1-2g/d, vancomycin-1-2g/d, metronidazole-500mg/d,
aminopenicillins-2-4g/d are alternative medications.

13. 13
ASSESSMENT
Based on the subjective and objective evidence the patient was
diagnosed as suffering from ‘GRADE-II ALCOHOLIC LIVER DISEADE
WITH HEPATIC ENCEPHALOPATHY’
Symptoms: Patient came with the complaints of fever since 3 months,
swellings of both feet since 10days gradually progressed to knee, loss of
appetite and sleep since 1wk.
Apparently asymptomatic 3months ago then he developed high grade
fever with chills, intermittent subsides with medications and relapses.
Risk factors: Chronic alcoholic – gudumba 1lit/day since 6yrs, non-smoker
having a habit of tobacco chewing since 15 yrs. Bowel and bladder
movements regular.
Diagnostic tests: S.BUN, LFT’s, S.Cr.
Which are as per text book.

14. Day wise assessment:
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VITALS D1 D2 D3 D4 D5 D6 D7 D8 D9 D10
TEMP 38 38 37 36 - - - - 36.7 37
BP[mmHg] 110/7
0
110/
70
120/
80
120/
70
110/
70
120/
70
120/8
0
110/
70
120/
70
120/
80
PULSE[bpm] 88 90 88 92 86 80 80 86 80 80
H/L NAD NAD NAD NAD NAD NAD NAD NAD NAD NAD
P/A Soft Soft Soft Soft soft soft Soft soft soft Soft
Fresh
complaints &
OTHERS
No
fresh
c/o
- - - - - - - - -

15. PLAN:
15
S.NO DRUGS DOSE
[mg]
ROA FREQ DURATION
Day of
admission
Day of
stopping
1 Lasix 20 IV BD D1 D10
2 Ceftriaxone 1000 IV BD D1 D10
3 PCM 500 PO TID D1 D10
4 PANTOP 40 IV OD D1 D10
5 UDILIV 300 PO BD D1 D10
6 MVT 500 PO BD D1 D10
7 ALBUMIN 25% IV OD q3rd
altr. day
D1 D10
8 ALDACTONE 100 PO OD D3 D10
9 ULTRACET PO OD D3 D10
Medication Dose ROA Frequency Duration of usage
Lactulose 1tsp PO BD 10d
PCM 500mg PO BD 10d
Discharge medication:

16. 16
DRUGS DOSE
[mg]
Category Use Monitoring parameters
Lasix 10-80 Diuretic pedal edema Electrolyte levels
Ceftriaxone 1000 Cephalosporin Reduce ammonia Dizziness, diaphoresis
PCM 500 Antipyretic Reduce fever Hepatotoxicity,
disorientation,hyperam
monia
PANTOP 40 PPI Reduce HCL
secretion
GI disturbances
UDILIV 300 Decrease
cholesterol
produced by liver
Dizziness, back pain,
abdominal pain
MVT 500 Nutrition
supplement
Neuropathy,
metabolic
functions
Constipation, dark stools
ALBUMIN 25g/25% Protein
[volume
expander]
Replaces plasma
protein
Edema, HTN
ALDACTONE 100 Diuretic Aldosterone
antagonist
Drowsiness, confusion

17. PHARMACIST INTERVENTIONS
 Checked for drug interactions, medication errors.
 Monitored signs and symptoms.
 Obtained patient history, including drug history and any known allergies, and
allergy to any of the drugs given.
 Monitored Blood pressure, Serum glucose, Serum urea levels, liver function tests;
incidence of seizures; renal function carefully during treatment.
 Monitor if the condition is progressing.
 No need for paracetamol.
 Monitor LFTS, CT-Scan, MRI, endoscopy every 6-12 months.
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Diagnosis and management Guidelines are according to the American
Association for the Study of Liver Diseases (AASLD) Practice Guidelines

18. PATIENT COUNSELING
About disease:
Hepatic encephalopathy is a brain dysfunction caused by liver
insufficiency and/or PSS; it manifests as a wide spectrum of neurological
or psychiatric abnormalities ranging from subclinical alterations to coma.
Symptoms include change in the behavior, confusion. drowsiness etc.
About medication’’]ns:
 Lactulose/lactitol: Lactulose and lactitol are disaccharides that are not
absorbed from the digestive tract. They are thought to decrease the
generation of ammonia by bacteria, render the ammonia inabsorbable
by converting it to ammonium (NH4+) ions, and increase transit of
bowel content through the gut.
Doses of 15-30 ml are administered three times a day; the result
is aimed to be 3–5 soft stools a day, or (in some settings) a stool pH of
<6.0.
 LOLA: A preparation of L-ornithine and L-aspartate (LOLA) is used to
increase the generation of urea through the urea cycle, a metabolic
pathway that removes ammonia by turning it into the neutral
substance urea. It may be combined with lactulose and/or rifaximin if
these alone are ineffective at controlling symptoms
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19. About life style modifications:
 Avoid greasy, spicy, caffeine containing food.
 Have more liquids; easily digested and; low carbohydrate food.
 Don’t use or stop any medications without doctors order.
 Follow healthy life style. Avoid alcohol and tobacco.
 Adhere to the medication regimen.
 High-protein foods to avoid include poultry, red meat, eggs, and fish.
 Consult physician if you observe any changes in your routine behavior.
 Eat well balanced diet with less protein and rich carbohydrate.[protein
required-0.8-1.2g/kg]
 Assess urinary status. If patient develops frequency, dysuria, edema or
reduced urinary output, notify physician.
 Assess for any changes in hepatic status. If patient appears jaundiced
and mentally confused, notify physician.
 If nausea, vomiting, distention, diarrhea or anorexia occur, pedal
edema, ascities, black stools notify physician.
 Limit your intake of food. Avoid sea foods.
 Consult physician if experience constipation. 19

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21. Thank you
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