1.
AKHIL JOSEPH
REG.NO : 13QO4O2

2.
 Cirrhosis is a slowly progressing disease in which
healthy liver tissue is replaced with scar tissue, eventually
preventing the liver from functioning properly. The scar
tissue blocks the flow of blood through the liver and
slows the processing of nutrients, hormones, drugs, and
naturally produced toxins.

3.
 As the disease worsens, a person may become
tired, weak, itchy, have swelling in the lower legs,
develop yellow skin, bruise easily, have fluid build up in
the abdomen, or develop spider-like blood vessels on the
skin. The fluid build-up in the abdomen may
become spontaneously infected. Other complications
include hepatic encephalopathy, bleeding from dilated
veins in the esophagus or dilated stomach veins, and liver
cancer. Hepatic encephalopathy results in confusion and
possibly unconsciousness.

4.
EPIDEMIOLOGY
 Cirrhosis is the ninth leading cause of death in the United
States and is responsible for 1.2% of all US deaths • Many
patients die in their fifth or sixth decade of life • The
prevalence is higher in non-Hispanic blacks and Mexican
Americans, those living below the poverty level, and those with
less than a 12th grade education • Each year, 2000 additional
deaths are attributed to fulminant hepatic failure (FHF), that
may be caused viral hepatitis, drugs (e.g., acetaminophen),
toxins (e.g., Amanita phalloides, the yellow deathcap
mushroom), autoimmune hepatitis, Wilson disease, or a variety
of less common etiologies. Cryptogenic causes are responsible
for one third of fulminant cases.

5.
ETIOLOGY
 It has many possible causes; sometimes more than one cause is
present in the same person. Globally, 57% of cirrhosis is
attributable to either hepatitis B (30%) or hepatitis C
(27%).Alcohol consumption is another important cause,
accounting for about 20% of the cases.
 Alcoholic liver disease (ALD). Alcoholic cirrhosis develops for
10–20% of individuals who drink heavily for a decade or more.
 Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in
the liver and eventually causes scar tissue.
 Chronic hepatitis C.
 Chronic hepatitis B.
 Primary biliary cirrhosis. Damage of the bile ducts leading to
secondary liver damage.

6.
 Primary sclerosing cholangitis. PSC is a progressive
cholestatic disorder presenting with
pruritus, steatorrhea, fat-soluble vitamin deficiencies,
and metabolic bone disease.
 Wilson's disease. Autosomal recessive disorder
characterized by low serum ceruloplasmin and
increased hepatic copper content on liver biopsy and
elevated 24-hour urine copper.
 Cystic fibrosis
 Hepatotoxic drugs or toxins
 Autoimmune hepatitis. This disease is caused by the
immunologic damage to the liver causing
inflammation and eventually scarring and cirrhosis.

7.
PATHOPHYSIOLOGY

8.
CLINICAL PRESENTATION
SYMPTOMS
 Gastrointestinal: bleeding, dark stool from digested blood,
fluid in the abdomen, nausea, passing excessive amounts of gas,
vomiting blood, or water retention
 Whole body: fatigue, loss of appetite, or reduced hormone
production
 Skin: web of swollen blood vessels in the skin or yellow skin
and eyes
 Weight: weight gain or weight loss
 Also common: swollen legs, yellow eyes, bleeding, breast
enlargement, breast enlargement in men (Gynecomastia),
bruising, dark urine, enlarged veins around belly button,
flapping hand tremor, itching, mental confusion, Poor
concentration and memory, muscle weakness, red palms,
swelling, swelling in extremities, or swollen veins in the lower
esophagus(Bleeding esophageal varices )

9.
ASCITES WITH PORTAL HYPERTENSION

10.
SIGNS
 Jaundice
 Scratch marks secondary to pruritus
 Spider angiomata/naevi (mainly found on the trunk and face)
 Skin telangiectasia's ('paper money skin')
 Palmar erythema
 Bruising
 Petechia or purpura
 Hair loss
 White nails (sign of hypoalbuminemia)
 Finger clubbing
 Dupuytren's contracture

11.
RISK FACTORS
 Obesity/overweight increases the risk for liver disease. Obesity
often results in the accumulation of fat cells in the liver. Acids
that are secreted by these fat cells (called fatty acids) can cause a
reaction in the body that destroys healthy liver cells and results
in scarring (sclerosis) and liver damage.
 The risk for developing liver disease varies, depending on the
underlying cause and the particular condition. General risk
factors for liver disease include alcoholism, exposure to
industrial toxins, heredity (genetics), and long-term use of
certain medications.
 Age and gender also are risk factors for liver disease. These
factors vary, depending on the particular type of disease. For
example, women between the ages of 35 and 60 have the highest
risk for primary biliary cirrhosis and men aged 30-40 are at
higher risk for primary sclerosing cholangitis.

12.
COMPLICATIONS
 Anemia, thrombocytopenia and coagulopathy (folate
deficiency, hemolysis, hypersplenism, cholestasis)
 Esophageal varices (portal hypertension)
 Ascites
 Spontaneous bacterial peritonitis
 Hepatocellular carcinoma
 Cirrhotic cardiomyopathy
 Hepatopulmonary syndrome
 Portopulmonary hypertension.

13.
DIAGNOSIS
 The gold standard for diagnosis of cirrhosis is a liver
biopsy, through
a percutaneous, transjugular, laparoscopic, or fine-needle
approach. A biopsy is not necessary if the clinical,
laboratory, and radiologic data suggests cirrhosis.
Furthermore, there is a small but significant risk to liver
biopsy, and cirrhosis itself predisposes for complications
caused by liver biopsy.The best predictors of cirrhosis are
ascites, platelet count <160,000/mm3, spider angiomata,
and Bonacini cirrhosis discriminant score greater than 7.

14.
normal liver tissue

15.
The liver in this histologic picture has wide bands of fibrous connective tissue separating
small islands of hepatic tissue.

16.
LAB FINDINGS
Thrombocytopenia - typically multifactorial. Due to alcoholic
marrow suppression, sepsis, lack of folate, sequestering in the
spleen as well as decreased thrombopoietin. However, this
rarely results in platelet count < 50 000/mL.
 Aminotransferases - AST and ALT are moderately elevated,
with AST > ALT. However, normal aminotransferases do not
preclude cirrhosis.
 Alkaline phosphatase - slightly elevated but less than 2-3 times
the upper limit of normal.
 Gamma-glutamyl transferase – correlates with AP levels.
Typically much higher in chronic liver disease from alcohol.
 Albumin - levels fall as the synthetic function of the liver
declines with worsening cirrhosis since albumin is exclusively
synthesized in the liver

17.
 Bilirubin - Levels normal when compensated but may elevate
as cirrhosis progresses.
 Prothrombin time - increases since the liver synthesizes
clotting factors.
 Globulins - increased due to shunting of bacterial antigens
away from the liver to lymphoid tissue.
 Serum sodium - hyponatremia due to inability to excrete free
water resulting from high levels of ADH and aldosterone.
 Leukopenia and neutropenia - due to splenomegaly with
splenic margination.
 Coagulation defects - the liver produces most of the
coagulation factors and thus coagulopathy correlates with
worsening liver disease.

18.
IMAGING
 Ultrasound is routinely used in the evaluation of cirrhosis.
It may show a small and nodular liver in advanced
cirrhosis along with increased echogenicity with irregular
appearing areas. Other findings suggestive of cirrhosis in
imaging are an enlarged caudate lobe, widening of the
liver fissures and enlargement of the spleen. An enlarged
spleen (splenomegaly), which normally measures less than
11–12 cm in adults, is suggestive of cirrhosis with portal
hypertension in the right clinical setting. Ultrasound may
also screen for hepatocellular carcinoma, portal
hypertension, and Budd-Chiari syndrome (by assessing
flow in the hepatic vein).
 Computed tomography (CT) scanning and/or magnetic
resonance imaging (MRI)

19.
ENDOSCOPY
 Gastroscopy (endoscopic examination of the esophagus,
stomach, and duodenum) is performed in patients with
established cirrhosis to exclude the possibility of
esophageal varices. If these are found, prophylactic local
therapy may be applied (sclerotherapy or banding)

20.
GRADING OF DISEASE
 The severity of cirrhosis is commonly classified with the Child-Pugh score.
This score uses bilirubin, albumin, INR, presence and severity of ascites,
and encephalopathy to classify patients in class A, B, or C. Class A has a
favourable prognosis, while class C is at high risk of death. It was devised
in 1964 by Child and Turcotte and modified in 1973 by Pugh and others.
Although it was originally used to predict mortality during surgery, it is now
used to determine the prognosis, as well as the required strength of
treatment and the necessity of liver transplantation.
 Modified Maddrey's discriminant function.
 The modified Maddrey's discriminant function) was originally described
by Maddrey and Boitnott to predict prognosis in alcoholic hepatitis. It is
calculated by a simple formula: (4.6 x (PT test - control))+ S.Bilirubin in
mg/dl
 Prospective studies have shown that it is useful in predicting short term
prognosis especially mortality within 30 days. A value more than 32 implies
poor outcome with one month mortality ranging between 35% to
45%. Corticosteroid therapy or pentoxifylline have been used with mixed
results for patients whose increased mortality is indicated with a value
greater than 32.

21.
SCORING
Points Class One year survival Two year survival
5–6 A 100% 85%
7–9 B 81% 57%
10–15 C 45% 35%
Measure 1 point 2 points 3 points
Total bilirubin, μmol/L
(mg/dL)
<34 (<2) 34–50 (2–3) >50 (>3)
Serum albumin, g/dL >3.5 2.8–3.5 <2.8
Prothrombin time,
prolongation (s)
<4.0 4.0–6.0 > 6.0
Ascites None
Mild (or suppressed
with medication)
Moderate to Severe
(or refractory)
Hepatic
encephalopathy
None Grade I–II Grade III–IV
The score employs five clinical measures of liver disease. Each measure is scored 1–3, with 3
indicating most severe derangement.
Chronic liver disease is classified into Child–Pugh class A to C, employing the added score
from above.
INTERPRETATION

22.
Modified Maddrey's discriminant function
 to predict prognosis in alcoholic hepatitis. It is calculated
by a simple formula:
 (4.6 x (PT test - control))+ S.Bilirubin in mg/dl.
 Prospective studies have shown that it is useful in
predicting short term prognosis especially mortality within
30 days. A value more than 32 implies poor outcome with
one month mortality ranging between 35% to 45%.

23.
DEMOGRAPHIC DETAILS OF
PATIENT
 NAME : XYZ
 SEX : Male
 DEPT : EICU
 DOA : 15-01-2017
 AGE : 56
 I.P NO : 1624
 UNIT :
 DOD : 24-01-2017

24.
REASON FOR ADMISSION:
 C/O bleeding from gums after tooth extraction.
 K/C/O alcoholic liver disease , admitted 6 months back.

25.
HISTORY OF PRESENT
ILLNESS:
 Pt was apparently alright 2 days back the he had tooth
extraction (3) following which he complains of bleeding
from gums. He also had C/O abdominal distension and
pedel edema.
 Abdominal distension since 6 months.
 K/C/O alcoholic liver disease, admitted for the same.
 H/O pedal edema - pitting type, no h/o fever, no h/o pain
in abdomen, no h/o vomiting of blood, no h/o passasge of
dark coloured stools.

26.
PAST MEDICAL HISTORY
Admitted for ALD six months back.
Not a K/C/O DM, HTN, TB, ASTHMA, EPILEPSY.
No H/O previous surgeries.

27.
Family history
 Diet : veg
 Sleep: disturbed
 Appetite : normal and regular.
 Habits : chronic alcoholic since 25 years, left 6 months
back.

28.
General physical examination.
 Pt is moderatly built and nourished.
 Not oriented to TPP.
ON EXAMINATION
 GC : fair
 Afebrile
 PR: 108 bpm
 BP: 110/70 mmHg
 SPO2 : 99%
+ + - - - +
 P I C K L E

29.
SYSTEMIC EXAMINATION
 CVS : S1 S2 +, NO MURMUR
 RS : B/L AE equal
 CNS : pt. drowsy
 P/A :palpation +
no local rise in temperature
non-tender
hepatomegaly +
inspection : distension +, umbilicus inverted.

30.
INVESTIGATIONS
 Complete hemogram with ESR
 LFT
 RBS
 Blood urea
 Serum electrolytes
 BT
 CT
 PT
 APTT
 INR
 Chest X-ray
 USG abdomen and pelvis.

31.
PROVISIONAL DIAGNOSIS
LIVER CIRROSIS ?

32.
LABORATORY FINDINGS
HB : 6.9 g/dl ↓ ( 13.5- 17.5 g/dl )
 WBC: 11,200 cells/µl. ↑
 RBC: 2.07Million/µl. ↓
 PLT: 1,12,000 cells/comm. ↓
 DLC: polymorphs: 78%
basophils: 00%
eosinophils : 02%
lymphocytes: 20%
monocytes: 00%
ESR : 120mm ↑ (<15mm)
Complete hemogram
 PCV : 17.2 % ( 40-50) ↓
 MCH : 33.3 pg ( 27-32) ↑
 MCHC : 40% ( 32- 46 )
 MCV : 83.3 fl ( 82 - 101)

33.
 ELECTROLYTES :
Sodium : 138 (135-147 mEq / L )
Potassium :3.8( 3.5-5.2 mEq / L )
Chlorides : 105 ( 95-107 mEq / L )
RBS: 106 mg/dl (60-140 mg/dl ).
HIV : Non-Reactive
HBsAg : NEGATIVE
HCV : NEGATIVE
BT : 3 mnts. 30 sec (1-6 min )
CT : 5min. 30sec ( 5-10 min )
PT: test : 20 sec , control : 13sec ↑
INR : 1.5 (0.8-1.1) ↑
APTT : test : 40sec, control : 22sec. ↑

34.
 PSS : normocytic normochromic anemia with
neutrophilia.
 Blood group : O+ve
RFT
 Sr. Urea : 32
 Creatinine : 0.7

35.
LFT
 ALT : 24 U/L (6-38)
 AST : 71 U/L ( 6-40) ↑
 ALP : 63 U/L ( 35-140)
 BILIRUBIN T : 7.3 MG% ( 0.2 – 1.0)↑
D : 2.8 MG% ( 0.1 - 0.4 ) ↑
I : 4.5 MG % ( 0.1 – 0.6)↑
Total protien : 6.7 ( 6.4-8.3 gm/dl)
Albumin : 2.9 ( 3.5 – 5 gm/dl ) ↓
Globulin : 3.8 ( 2.3 – 3.5 gm/dl) ↑
A/G ratio : 1:1.3
Ammonia : 68mcg/dl ( 9.5-49) ↑

36.
Ascitic fluid examination
 Protien : 1.5 gm %
 Chloride : 120mEq/L
 Sugar : 173mg%
 Gram stain : Few lymphocytes seen, no organisms.
 ZN stain : No AFB

37.
URINE ROUTINE
 Pus cells : 1-2/ hpf
 Epithelial cells : 1-2/hpf

38.
USG ABDOMEN
 1. CIRRHOSIS OF LIVER WITH PORTAL
HYPERTENSION AS EVIDENCED BY
SPLEENOMEGALYAND GROSS TENSE ASCITES.
 2. CHOLELITHIASIS

39.
TREATMENT CHART

40.
BRAND
NAME
GENERIC NAME DOSE ROUTE FREQUENCY
D
A
Y
1
D
A
Y
2
D
A
Y
3
D
A
Y
4
D
A
Y
5
D
A
Y
6
D
A
Y
7
D
A
Y
8
D
A
Y
9
D
A
Y
10
IVF
NS
DNS WITH 2
AMP
OPTINEURON
2 PINT
1 PINT
IV
1-0-0-1
√
√
√
√
√
√
√ √ √
√ √ √ √
INJ. XONE CEFTRIAXONE 1 GM IV 1-0-1 √ √ √ √ √
TAB OFLOX OFLOXACIN 400MG P/O 1-0-1 √ √ √ √ √
INJ. PAN PANTOPRAZOL
E
40 MG IV 1-0-0 √ √ √ √ √ √ √ √ √ √
INJ.
VITAMIN K
VITAMIN K IM 1-0-1 √ √ √ √ √ √
INJ.
HEPAMERZ
L-ORNITHINE
L-ASPARTATE
I AMP
IN 100
MLNS
1-1-1
2-2-2 (SACHET)
√ √ √
√ √
1-
1-
1 √ √ √ √
INJ. EMSET ONDANSTRON 4 MG IV 1-1-1 √ √ √
TAB.
UDIBON
URSODEOXYCH
OLIC ACID
SILYMARIN
300MG
140MG
P/O 1-0-1 √ √ √ √ √ √ √ √ √ √
INJ. PAUSE TRANEXAMIC
ACID
I AMP
IN 100
ML NS
1-0-1 √ √ √ √ √ T
A
B
√
SYP.DUPHAL
AC
LACTULOSE 15ML P/O 1-1-1 √ √ √ √ √ √ √ √ √ √

41.
BRAND
NAME
GENERIC NAME DOSE ROUTE FREQUENCY
D
A
Y
1
D
A
Y
2
D
A
Y
3
D
A
Y
4
D
A
Y
5
D
A
Y
6
D
A
Y
7
D
A
Y
8
D
A
Y
9
D
A
Y
10
TAB. DYTOR
PLUS
TORASEMIDE
SPIRONOLACTO
NE
10 MG
50 MG
P/O 1-0-0 √ √ √ √ √
INJ. 25%
DEXTROSE
DEXTROSE IV 1-1-1 √ √ √ √
TAB.
RIFAGUT
RIFAXIMIN 400MG P/O 1-1-1 √ √ √ √ √ √ √ √ √
INJ.
OCTREOTID
E
OCTREOTIDE
ACETATE
5 AMP
IN 1OO
ML NS
IV @ 30ML / HR √ √
INJ.METRO
GYL
METRONIDAZO
LE
100ML IV 1-1-1 √ √ √ √ T
H. ALBUMIN HUMAN
ALBUMIN
100 ML IV 1-0-0 √
SYP.
POTKLOR
KCL 2TSP P/O 2 TSP WITH
WATER
√ √ √ √ √ √
TAB.
OROFER XT
TOTAL
ZN, FOLIC
ACID,ELEMENT
AL IRON,
METHYLCOBAL
AMIN
22.5MG
1.1MG
100MG1
.55MG
P/O 0-1-0
√ √ √
Β- PROTIEN
POWDER PROTIENS
2 TSP
WITH
MILK
P/O 1-1-1 √

42.
FOLLOW UP
 DAY 1
 PR : 120bpm
 BP: 130/70 mmhg
O/E
 afebrile
S/E
 Pt is conscious and oriented.
 CVS : S1S2 +
 RS : B/L AEE
 CNS : irritable and drowsy
 P/A : hepatomegaly
 1 PINT PCV TRANSFUSED

43.
Abdominal Girth : 94cm
Oral suctioning – hourly
RT FEED : 100ML 1-1-1-1

44.
ADVICE
 INJ. METROGYL 100ML IV 1-1-1
 INJ. XONE 1GM IV 1-0-1
 INJ. PAN 40 MG IV 1-0-0
 INJ. VITAMIN K 1 AMP IN 100ML NS IV 1-0-1
 INJ. HEPAMERZ 2 AMP IN 100ML NS IV 1-1-1
 INJ. EMSET 4MG IV 1-1-1
 TAB. UDIBON 1-0-1
 INJ. Pause 1 AMP IN 100ML NS 1-0-1
 SYP. DUPHALAC 2 TSP √-√-√
 INJ. 25% DEXTROSE 1-1-1
 DUPHALAC BOWEL WASH 1-1-1-1-1-1
 INJ. 1 PINT DNS WITH 2 AMP OPTINEURON 1-0-0-1
 TAB. RFAGUT 400MG 1-1-1
 INJ. OCTREOTIDE 5AMP IN 1 PINT NS @ 30ML/ HR

45.
DAY 2
Pt on Mechanical Ventilation
BP: 120/80 mmhg
PR: 92 bpm
Systemic examination
CNS : conscious and oriented, B/L PERL +
CVS : s1s2 +
P/A : soft, distended.
Spo2 : 98%

46.
Investigations (17-01-2017)
 Hb : 7.2
 PT: T : 23.8 sec
C: 13.5 sec
INR: 1.86
APTT
T: 28 sec
C: 22 sec
Creatinine : 1.0
 Treatment
As Per Chart.

47.
Day 3
 No fresh complaints.
 PR: 72 bpm
 BP: 110/80 mmhg
 SPO2: 98%
 CNS: conscious and oriented. Flaps +
 RS: B/L AEE
 CVS: s1s2 +
 P/A: soft, distented. Free fluid +
 Abdominal Girth : 91cm

48.
Investigations
HB : 6.6 g/dl ↓ ( 13.5- 17.5 g/dl )
 WBC: 4800 cells/µl.
 RBC: 2.04Million/µl. ↓
 PLT: 73,000 cells/comm. ↓
 DLC: polymorphs: 72%
basophils: 00%
eosinophils : 03%
lymphocytes: 25%
monocytes: 00%
 ELECTROLYTES :
Sodium : 144 (135-147 mEq / L )
Potassium :2.9 ( 3.5-5.2 mEq / L )
Treatment
 As per chart

49.
Day 4
No fresh complaints
PR: 88bpm
BP: 110/80 mmhg
Spo2 : 96%
CNS : conscious and oriented
RS : B/L AEE
CVS: s1 s2 +
P/A: soft, distended.

50.
Investigations
 Potassium : 2.9 mEq/L
CHILD PUGH SCORE
 Score : 11
 CLASS – C
 1 YR MORTALITY – 55% , Two year survival – 35%
Modified Maddrey's discriminant function – 54.7
TREATMENT
 1 pint PCV transfused.
 As per chart.

51.
Day 5
 Patient shifted to wards
 No fresh complaints
 PR: 86 bpm
 BP: 114/76 mmhg
 CNS: conscious and oriented
RS: B/L AEE
CVS: S1S2 +
P/A: soft, distented.
 Abdominal Girth : 90cm

52.
Investigations
 Potassium : 3.1 mEq/L
TREATMENT
 1 pint PCV transfused
 As per chart.

53.
Day 6
 No fresh complaints
 PR: 82 bpm
 BP: 108/70 mmhg
CNS: conscious and oriented
RS: B/L AEE
CVS: S1S2 +
P/A: soft, distented, non-tender.

54.
Investigations
HB : 7.9 g/dl ↓ ( 13.5- 17.5 g/dl )
 WBC: 5,100 cells/µl. ↓
 RBC: 2.47Million/µl. ↓
 PLT: 74,000 cells/comm. ↓
 DLC: polymorphs: 60%
basophils: 00%
eosinophils : 04%
lymphocytes: 34%
monocytes: 02%
RFT
 Sr. Urea : 24
 Creatinine : 1.0
TREATMENT
 As per chart.

55.
Day 7
 No fresh complaints
 PR: 88 bpm
 BP: 110/70 mmhg
CNS: conscious and oriented
RS: B/L AEE
CVS: S1S2 +
P/A: soft, distented, non-tender.
Abdominal Girth : 90cm

56.
Investigations
 ELECTROLYTES :
Sodium : 136 (135-147 mEq / L )
Potassium :4.1( 3.5-5.2 mEq / L )
Chlorides : 101 ( 95-107 mEq / L )
LFT
 ALT : 22 U/L (6-38)
 AST : 57 U/L ( 6-40)
 ALP : 49 U/L ( 35-140)
 BILIRUBIN T : 4.6 MG% ( 0.2 – 1.0)
D : 1.4 MG% ( 0.1 - 0.4 )
I : 3.2 MG % ( 0.1 – 0.6)
Total protien : 5.9
Albumin : 2.0
Globulin : 3.9
A/G ratio : 1:1.9

57.
 TREATMENT
 1 pint PCV transfused
 As per chart.

58.
Day 8
 No fresh complaints
 PR: 86 bpm
 BP: 108/74 mmhg
CNS: conscious and oriented
RS: B/L AEE
CVS: S1S2 +
P/A: soft, distented, non-tender.
Abdominal Girth : 88cm

59.
Treatment Advice
 1 pint PCV transfused.
 As per chart.

60.
Day 9
 No fresh complaints
 PR: 84 bpm
 BP: 130/90 mmhg
CNS: conscious and oriented
RS: B/L AEE
CVS: S1S2 +
P/A: soft, distented, non-tender.
Abdominal Girth : 87cm

61.
Investigations
HB : 8.3 g/dl ( 13.5- 17.5 g/dl )
 WBC: 5,300cells/µl.
 RBC: 2.54Million/µl.
 PLT: 1,50,000 cells/comm.
 DLC: polymorphs: 70%
basophils: 00%
eosinophils : 02%
lymphocytes: 208
monocytes: 00%
ESR : 42 mm (<15mm)
Complete hemogram
 PCV : 23.3 % ( 40-50)
 MCH : 32.5 pg ( 27-32) ↑
 MCHC : 35.4% ( 32- 46 )
 MCV : 92 fl ( 82 - 101)

62.
PT
test : 14 sec ,
control : 13sec
INR : 1.0 (0.8-1.1)
APTT
test : 28sec,
control : 22sec.
Peripheral Smear Study
Impression : NORMOCYTIC HYPOCHROMIC ANEMIA

63.
 UPPER GI ENDOSCOPY
Impression : GRADE II OESOPHAGEAL VARICES
WITH CONGESTIVE GASTROPATHY.
Patient attendees are not willing for surgical intervention /
banding.
 TREATMENT
AS PER CHART.

64.
ESOPHAGEAL VARICES CONGESTIVE GASTROPATHY

65.
Final Diagnosis
 CIRRHOSIS OF LIVER WITH PORTAL
HYPERTENSION, HEPATIC ENCEPHALOPATHY
AND GRADE II OESOPHAGEAL VARICES WITH
CONGESTIVE GASTROPATHY.

66.
DISCHARGE MEDICATION
BRAND
NAME
GENERIC NAME DOSE ROUTE FREQUENC
Y
DURATION
TAB. PAN PANTOPRAZOLE 40MG P/O 1-0-0 15 DAYS
TAB. UDIBON URSEODEOXYCHOLIC ACID
SILYMARIN
300MG
140MG
P/O 1-0-1 15 DAYS
TAB. RIFAGUT RIFAXIMIN 400MG P/O 1-1-1 15 DAYS
HEPAMERZ
SACHET WITH
WATER
L-ORNITHINE L-ASPARTATE 3 GM P/O 1-1-1 15 DAYS
TAB. DYTOR PLUS TORASEMIDE
SPIRONOLACTONE
10 MG
50MG
P/O 1-1-0 15 DAYS
SYP. DUPHALAC LACTULOSE 10ML P/O 1-1-1 15 DAYS
B-PROTIEN
POWDER WITH
MILK
PROTIEN 2 TSP P/O 1-1-1 15 DAYS
TAB. OROFER XT
TOTAL
ZN,
FOLIC ACID,
ELEMENTAL IRON,
METHYLCOBALAMIN
22.5MG
1.1MG
100MG
1.55MG
P/O 0-1-0 15 DAYS

67.
REVIEW
 Review in medical OPD on WEDNESDAY after 15 days
or incase of any emergencies.

68.
PHARMACEUTICAL CARE PLAN

69.
SUBJECTIVE EVIDENCES
 C/O bleeding from gum after tooth extraction.
 K/C/O alcoholic liver disease , admitted 6 months back.
 Abdominal distension since 6 months.
 B/L pedel edema – pitting type.

70.
OBJECTIVE EVIDENCES
HB : 6.9 g/dl ↓ ( 13.5- 17.5 g/dl )
 WBC: 11,200 cells/µl. ↑
 RBC: 2.07Million/µl. ↓
 PLT: 1,12,000 cells/comm. ↓
 ESR : 120mm ↑ (<15mm)
PT: test : 20 sec , control : 13sec ↑
INR : 1.5 (0.8-1.1) ↑
APTT : test : 40sec, control : 22sec. ↑
PSS : normocytic normochromic anemia with neutrophilia.

71.
LFT
 ALT : 24 U/L (6-38)
 AST : 71 U/L ( 6-40) ↑
 ALP : 63 U/L ( 35-140)
 BILIRUBIN T : 7.3 MG% ( 0.2 – 1.0)↑
D : 2.8 MG% ( 0.1 - 0.4 ) ↑
I : 4.5 MG % ( 0.1 – 0.6)↑
USG ABDOMEN
 1. CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION AS EVIDENCED
BY SPLEENOMEGALY AND GROSS TENSE ASCITES.
 2. CHOLELITHIASIS
UPPER GI ENDOSCOPY
Impression : GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE
GASTROPATHY.

72.
ASSESSMENT
 BY OBSERVING THE SUBJECTIVE AND OBJECTIVE
EVIDENCES THE PATIENT WAS DIAGNOSED AS
CIRRHOSIS OF LIVER WITH PORTAL
HYPERTENSION, HEPATIC ENCEPHALOPATHY AND
GRADE II OESOPHAGEAL VARICES WITH
CONGESTIVE GASTROPATHY.

73.
PLANNING
GOALS TO BE ACHIEVED
 To improve patients quality of life.
 To prevent further progress of complications.
 To reduce the gum bleeding.
 To normalise the blood counts.
 To reduce the ESR level.
 To reduce the abdominal distension.
 To reduce mortality rate.

74.
GOALS ACHIEVED
 Patients quality of life improved.
 Minimised the further progress of complications.
 Gum bleeding stopped.
 Blood counts and levels are improving.
 ESR level is decreased.
 Abdominal distension reduced.

75.
MONITORING PARAMETERS
 CBC with complete hemogram.
 ESR
 LFT
 Prothrombin time and INR
 Ascites, abdominal distension, bleeding.
 Sign and symptoms.

76.
PHARMACIST INTERVENTION
 Major drug-drug interactions.
 POTASSIUM CHLORIDE – SPIRONOLACTONE
Concurrent use of potassium and spironolactone may results in
hyperkalemia.
 METRONIDAZOLE-ONDANSETRON,
 OCTREORIDE ACETATE- OFLOXACIN
 ONDANSETRON- OCTREORIDE ACETATE
 OFLOXACIN - ONDANSETRON
 METRONIDAZOLE – OFLOXACIN
 METRONIDAZOLE - OCTREORIDE ACETATE, all these
maycauses QT interval prolongation.

77.
 Moderate drug-drug interactions
 ceftriaxone torsemide
Cephalosporin antibiotics like cefTRIAXone can occasionally
cause kidney problems, and using it with torsemide may
increase that risk. The interaction is more likely to occur when
the cephalosporin is given at high dosages by injection into the
vein or when it is given to the elderly or individuals with
preexisting kidney function impairment.
 ofloxacin lactulose
Ofloxacin can cause an irregular heart rhythm that may be
serious and potentially lifethreatening, although it is a
relatively rare side effect. The risk is increased if you have low
blood levels of magnesium or potassium, which can occur with
bowel cleansing preparations or excessive use of medications
that have a laxative effect.

78.
 Torsemide - Pantoprazole
Using pantoprazole together with torsemide may cause a
condition called hypomagnesemia, or low blood
magnesium. Drugs known as proton pump inhibitors
including pantoprazole can cause hypomagnesemia when
used for a prolonged period.
Banding has to be done to prevent the rupture of
esophageal varices, rupture and bleeding further lead to
more complications and increased mortality rate.

79.
PATIENT COUNSELLING
ABOUT DISEASE ;
 Cirrhosis is a slowly progressing disease in which
healthy liver tissue is replaced with scar tissue, eventually
preventing the liver from functioning properly. The scar
tissue blocks the flow of blood through the liver and
slows the processing of nutrients, hormones, drugs, and
naturally produced toxins.
 Portal hypertension is an increase in the blood pressure
within a system of veins called the portal venous system.
Veins coming from the stomach, intestine, spleen, and
pancreas merge into the portal vein, which then branches
into smaller vessels and travels through the liver.

80.
 Hepatic encephalopathy (HE) is the occurrence of confusion,
altered level of consciousness, and coma as a result of liver
failure. In the advanced stages it is called hepatic coma. It may
ultimately lead to death. It is caused by accumulation in the
bloodstream of toxic substances that are normally removed by
the liver.
 Esophageal varices are extremely dilated sub-
mucosal veins in the lower third of the esophagus. They are
most often a consequence of portal hypertension, commonly
due to cirrhosis; patients with esophageal varices have a
strong tendency to develop bleeding.

81.
 Portal hypertensive gastropathy ( congestive
gastropathy ) refers to changes in the mucosa of
the stomach in patients with portal hypertension ; by far
the most common cause of this is cirrhosis of the liver.
These changes in the mucosa include friability of the
mucosa and the presence of ectatic blood vessels at the
surface.

82.
ABOUT MEDICATION
 Take medications on time.
 Don’t skip the medication.
 Pantoprazole can be taken with or without food.
 Rifaximin can be taken with or without food.
 Udibon has to be taken with food.
 Hepamerz sachet dissolved in a glass of water and taken
after the meals.
 Lactulose can be taken either with or without food.
However, if you find it makes you feel sick this can be
reduced by taking it with water, fruit juice or meals. You
can take lactulose undiluted, or you can mix the required
dose of lactulose into a drink of water or fruit juice.
 Swallow each dose straight away. Don't keep it in your
mouth as the sugar content may lead to tooth decay

83.
LIFE STYLE MODIFICATIONS
 Lifestyle changes cannot cure cirrhosis, but they can help to delay or
stop progression of the disease, reduce the severity of symptoms, and
help prevent complications.
 Avoid drinking alcohol.
 Eat a balanced diet.
 Avoid raw seafood.
 Discuss the appropriate amount of protein you need to eat, an adult who
weighs 68 kilograms needs at least 54 grams of protein each day
 Depending on your condition, you may either need to increase or
decrease protein intake.
 Take any vitamin or mineral supplements recommended by your doctor.
 A low-salt diet may be needed to reduce fluid retention.
 Get your doctor’s approval for all medicines. For
example, acetaminophen (such as Tylenol) can speed up liver
damage. Aspirin and other nonsteroidal anti-inflammatory drugs
(NSAIDs)-for example, ibuprofen and naproxen -increase the risk
of variceal bleeding if you have enlarged veins (varices) in the
digestive tract.

84.
 Get vaccines for flu, pneumonia, and hepatitis.
 Put your feet up to reduce swelling.
 Be careful with herbs and dietary supplements. Herbal
remedies, herbal combinations and dietary supplements aren’t
subject to the same approval process as medication and some
may harm the liver. A few that have caused liver problems are
cascara, chaparral, comfrey, kava and ephedra.
 Stop smoking. Quitting tobacco use will improve your overall
health, which may help make you a better candidate for a liver
transplant if you need one.
 Increased caffeine consumption is most beneficial for people
who are at high risk for developing chronic liver disease, It's
important to note if you already have cirrhosis, coffee isn’t
powerful enough to reverse damage

85.
STANDARD TREATMENT
Complication Treatment Approach Monitoring
Parameter
Outcome Assessment
Ascites Diet, diuretics,
paracentesis,
Daily assessment of
weight
Prevent or eliminate
ascites and its
secondary
complications
Variceal bleeding Pharmacologic
prophylaxis Endoscopy,
vasoactive drug therapy
(octreotide),
ligation or sclerotherapy,
volume resuscitation,
pharmacologic
prophylaxis
Child-Pugh score,
endoscop, CBC,
evidence of overt
bleedingy, CBC
Acute: control acute
bleed
Chronic: variceal
obliteration, reduce
portal
pressures
Hepatic
encephalopathy
Ammonia reduction
(lactulose, cathartics),
elimination
of drugs causing CNS
depression, limit
excess protein in diet
Grade of
encephalopathy, EEG,
psychological
testing, mental status
changes, concurrent
drug therapy
Maintain functional
capacity, prevent
hospitalization
for encephalopathy,
decrease ammonia
levels, provide
adequate nutrition

86.
LIVER TRANSPLANTATION
 The complications seen in patients with chronic liver disease are
essentially functional as a secondary effect of the circulatory and
metabolic changes that accompany liver failure. Consequently,
liver transplantation is the only treatment that can offer a cure for
complications of end-stage cirrhosis. However, patient selection,
evaluation, and pre- and postsurgical management are beyond the
scope of this review. The surgical procedure is very demanding
and ranges from 4 to 18 hours depending on outcome.
Numerous anastomoses and sutures, and many disconnections
and reconnections of abdominal and liver tissue, must be made
for the transplant to succeed, requiring an eligible recipient and a
well-calibrated live or cadaveric donor match. The large majority
of liver transplants use the entire liver from a non-living donor
for the transplant, particularly for adult recipients. A major
advance in pediatric liver transplantation was the development of
reduced size liver transplantation, in which a portion of an adult
liver is used for an infant or small child

87.
Liver donor requirements
 Any member of the family, parent, sibling, child, spouse or a
volunteer can donate their liver. The criteria for a liver donation
include:
 Being in good health
 Having a blood type that matches or is compatible with the
recipient's, although some centres now perform blood group
incompatible transplants with special immuno suppression protocols
 Having a charitable desire of donation without financial motivation
 Being between 18 and 60 years old
 Being of similar or bigger size than the recipient
 Before one becomes a living donor, the donor must undergo testing
to ensure that the individual is physically fit. Sometimes CT scans or
MRIs are done to image the liver. In most cases, the work up is done
in 2–3 weeks.

88.
Band Ligation / Banding
 Endoscopy band ligation is used to treat enlarged veins in the
esophagus, the tube connecting the throat to the stomach. If left
untreated esophageal veins (varices) can spontaneously rupture and
cause severe bleeding.
 The procedure is performed during an upper gastrointestinal
endoscopy. A local anesthetic is given to numb the throat and sedation
medication will also be given through IV to help you relax/sleep
through the procedure.
 A scope is placed in the mouth down to the esophagus. When varices
are found, tiny elastic bands are placed around the enlarged veins in
the esophagus to tie them off so they can’t bleed. The banded varices
are then eventually sloughed after a few days and the esophagus is
much less likely to bleed after it’s healed.