Esophageal Varices

Clinical Pharmacy Week 4: Tingkat 2 & 3

By
Liew Hui Lian (PRP)
2009/2010
 Outline

Esophageal Varices
− What is it?
− Classification
− Epidemiology
− Risk factors
− Clinical manifestation
− Management


Case Study
 What is it?

Very dilated submucosal vein in the lower
esophagus – like internal varicose veins

Due to portal hypertension, most commonly
from liver cirrhosis

Normally, veins are 1 mm in diameter and
becomes distended to 1-2 cm in diameter

Most likely 5-8% patients who are diagnosed
liver cirrhosis develop EV.

Varices size increase 10-15% annually.
 Classification
Japanese US VA Paquet
Japanese US TrialPaquet
VA Trial
Absent Absent Absent I
Grade 1: small, straight varices not disappearing with insufflation
Absent smal
Absent< 5 mmAbsent II I
Grade 2: medium varices occupying less than one third of the lumen medium 5-9 mm III
Grade
Grade 3: large varices
1: small, straightoccupying
varicesmorenotthan one third of the
disappearing lumen
with large
smal > 9 <mm
5 mmIV II
insufflation
Grade 2: medium varices occupying less than one third of the mediu 5-9 mm III
lumen m
Grade 3: large varices occupying more than one third of the large > 9 mm IV
lumen

* The Japanese Classification is the preferred grading scale for the staging of oesophageal
Varices.
• 30% will experience haemorrhage
• Risk is greatest during first year of diagnosis
• Mortality 30-50% within 6 weeks
• Those that survive first bleed are at significant
risk of recurrent haemorrhage (70%) and a
third are fatal
• Risk of re-bleeding: hepatic decompensation,
age >60, severity of initial bleed, renal
insufficiency, level of portal pressure, size of
varices, presence of hematoma
 Epidemiology
• Prevalence in patient with cirrhosis 24-81%
• Variceal bleeding accounts for 6.4% of upper
gastrointestinal bleeding in Malaysia.
• 15% of emergency endoscopy for UGIB in
Selayang Hospital are due to acute variceal
bleeding.
• Aetiology in Malaysia mainly: hepatitis B or
alcohol
• Majority of patients are Chinese, followed by
Indians
 Risk Factors

Severity of liver dysfunction

Size of varices

Presence of endoscopic red wale signs

Hepatic venous pressure gradient (HVPG).
Bleeding is likely if it's above 12 mmHg
• For patients with cirrhosis
• American College of Gastroenterology and the
American Association for the Study of Liver
Disease
– No varices: Every other year
– Small varices: every 1-2 years

Screening Endoscopy
 OGDS view

1. Normal
2. Variced esophageal
3. Bleeding varices
 Clinical Manifestation

Anemia

Coughing up or vomitting blood

Black tarry stools due to bleeding in the gut

Lightheadedness from the loss of blood

Passing out from the lost of blood
• Non selective B adrenergic antagonist (e.g.
propanolol and nadolol)
– Prevents splanchnic vasoconstriction
– Reduce risk of bleeding by 45%
– Propanolol is the most cost effective
• Nitrates
– Reduces portal pressure
– But ineffective in preventing bleeding in patients
as monotherapy

Pharmacological Therapy
 • Variceal ligation

Endoscopic Therapy
 • Injection sclerotherapy

Endoscopic Therapy
 Management
Hypovolumic shock: Blood transfusion of pack
cells
rd
Bacterial infections : Antibiotic (3 generation
cephalosporin or quinolones i.e. norfloxacin/
ciprofloxacin) 7 days prophylaxis
• Effective to stop bleeding but have high re-bleeding rate and other complications
(ulceration, perforation and aspiration pnewmonia).
• Only for when no endoscopy is not available.

Balloon Tamponade
Rescue therapy for uncontrolled variceal bleeding after combined pharmacological and
endoscopic therapy.

Transjugular Intrahepatic
Portosystemic Shunts (TIPS)
Case Study
 Patient's profile

Name: NDNK

MRN: 28116

Age: 46

Gender: M

Race: Siamese

Weight: 70 kg

DOA: 9 November 2009

DOD: 12 November 2009

Ward/ Bed: T2/311

Chief Complaint:
− Passing black stool and abdominal discomfort
and pain


History of Present Illness
− Passing of black stool 2/7 and hematemesis 1
time today
− No fresh blood or spitting black blood
− Mild headache
− Soft and tender at epigastric region
• Past Medical History
– k/c/o Hepatitis C
– OGDS done in June 2009 at Sungai Petani hospital,
and was diagnosed with having esophageal varices.

Review of System
− BP: 110/60
− PR: 86 /min
− RR: 21 /min
− T: 37 C


Social/ Family History
− Smokes 1 pack of cigarette per day
− Married and lives with wife

Past Medication History
− None


Compliance evaluation
− Not applicable

Diagnosis/ Surgical Procedure
− UGIB 2nd to esophageal varices 2nd to portal
hypertension
− Grade 1 large bleeding
 Laboratory Results
Normal Day 1 Day 2* Day 3 Day 4
Range
TWBC 4-11 x 10 L 12.0 15.6 14.4 5.9

HB 11.5-16.5 8.6 6.9 8.6 9.0

g/100ml

RBC 4.5-6.3 x 106 2.8 2.3 2.9 3.0

HCT 0.4/0.37- 6.3 21.7 26.3 27.7

0.52/0.48

Platelet 150-400x 107 127 96 72

10/L

* 2 pints of PC were transfused that day

 Laboratory Results
Normal Day 1 Day 2 Day 3 Day 4
Range
Urea 1.7-8.3 11.1 10.8
mmol/L
Na 135-145 138 140
mmol/L
K 3.5-5.0 4.1 4.8
mmol/L
Ca 2.1-2.6
mmol/L
Mg 0.7-1.3
mmol/L
PO4- 0.8-1.45
mmol/L
Scr 64-122 umol/L 83
 Laboratory Results
Normal Day 1 Day 2 Day 3 Day 4
Range
Albumin 35-50 g/L 29

T. < 20 umol/L 27.9

Bilirubin

T. Protein 66-87 g/L 64

ALP 53-141 u/L 88

ALT < 32 u/L 56

 Laboratory Results

Normal Range Day 1 Day 2 Day 3 Day 4

PT 10-13.5 sec 14.7

APTT 26-42 sec 37.1

INR < 1.5 1.35

 Laboratory Results

Normal Range Day 1 Day 2 Day 3 Day 4

CK 24-195 u/l
LDH 0-248 u/L
AST <37 60
 Daily Monitoring

Normal Day 1 Day 2 Day 3 Day 4

Range

BP 110/60 100/60 110/61 138/80

Temp 37 C 37 38 37 37
RR 12-18/ min 20 20 20 21

PR 60-100/min 86 94 62 70
 Medication

Dose Frequency D1 D2 D3 D4
Cardiovascular
T. Propanolol 40 mg STAT, BD 1/52 Y Y Y Y

Others
IV Pantoprazole 40 mg STAT, BD 1/52 Y Y Y Y
S/C Sandostatin 0.1 mg STAT, TDS 1/52 Y Y Y
(Octreotide)
 Clinical Progress

Day 1 
Plan
− Passing black stool 2/7 − Start IV 3 pint D5, 2 pint
a/w hematemesis once NS
today − ICNBN
− No fresh blood, spitting − For OGDS tomorrow
black mouth/ blood.
− Start IV pantoprazole 30
− No SOB, no chest pain,
mg BD
no diarrhea.
− T. Propanol 40 mg BD
− Abdomen discomfort and
pain
− OE: Alert and conscious
− Sclera or conjunctiva no
jaundice
− Skin tugor good
− CVS: DRNM
 Clinical Progress
• Day 2 
Plans:
– Lethargy − OGDS today
– PU normal − KNBM
– has flatus − Cont. IV 2 pint NS and 3
pints D5
– PR showed fresh malena
– Refused CBD insertion
 Clinical Progress

Day 3 
Plan
− BO with fresh malena − Cont KNBM
− PU normal − Cont IVD 5 pint (2NS, 3
D5)
− Cont . 2 pack cell for
transfusion
− Cont. v/s monitoring
 Clinical Progress

Day 4 
Plan
− − Discharge today
PU
− − Syrup lactulose 30 mls
PR = fresh blood
ON
− T propanolol 40 mg BD
− TCA 1/12 with
rebanding
 Discharge Medication

Syrup Lactulose 30 mls ON 1/52
– To prevent hepatic encephalopathy
– Causes osmotic diarrhea, thus lessening the time
available for intestinal bacteria to metabolize prot. It
also acidifies the environment which promotes the
conversion of lumenal ammonia to ammonium, which
lessen absorption in the gut.

T. Propanolol 40 mg BD 1/12
– Causes vasoconstriction, thus reducing splanchnic
blood flow


TCA:
– 1/12 with rebanding
– OGDS on 7 December 2009
The End.... :D