Esophageal Varices Week 4 T2t3

Esophageal Varices

Clinical Pharmacy Week 4: Tingkat 2 & 3 By Liew Hui Lian (PRP) 2009/2010

Outline 



Esophageal Varices −

What is it?

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Classification

−

Epidemiology

−

Risk factors

−

Clinical manifestation

−

Management

Case Study

What is it? 

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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 Japanese Absent Grade 1: small, straight varices not disappearing with insufflation Absent Grade 2: medium varices occupying less than one third of the lumen Grade 3: large varices occupying one third of the lumen Grade 1: small, straight varicesmore notthan disappearing with

US

VA Paquet VA Trial TrialPaquet

US Absent Absent I smal Absent< 5 mm Absent II medium 5-9 mm III large smal > 9 <mm 5 mmIV

I II

insufflation Grade 2: medium varices occupying less than one third of the lumen

mediu m

5-9 mm

III

Grade 3: large varices occupying more than one third of the lumen

large

> 9 mm

IV

* 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

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Size of varices

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Presence of endoscopic red wale signs

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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

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Coughing up or vomitting blood

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Black tarry stools due to bleeding in the gut

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Lightheadedness from the loss of blood

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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

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MRN: 28116

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Age: 46

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Gender: M

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Race: Siamese

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Weight: 70 kg

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DOA: 9 November 2009

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DOD: 12 November 2009

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Ward/ Bed: T2/311

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Chief Complaint: −

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Passing black stool and abdominal discomfort and pain

History of Present Illness −

Passing of black stool 2/7 and hematemesis 1 time today

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No fresh blood or spitting black blood

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Mild headache

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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.

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Review of System −

BP: 110/60

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PR: 86 /min

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RR: 21 /min

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T: 37 C

Social/ Family History −

Smokes 1 pack of cigarette per day

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Married and lives with wife

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Past Medication History −

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None

Compliance evaluation −

Not applicable

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Diagnosis/ Surgical Procedure −

UGIB 2nd to esophageal varices 2nd to portal hypertension

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Grade 1 large bleeding

Laboratory Results Normal Range

Day 1

Day 2*

Day 3

Day 4

TWBC

4-11 x 10 L

12.0

15.6

14.4

5.9

HB

11.5-16.5 g/100ml

8.6

6.9

8.6

9.0

RBC

4.5-6.3 x 106

2.8

2.3

2.9

3.0

HCT

0.4/0.370.52/0.48

6.3

21.7

26.3

27.7

Platelet

150-400x 10/L

107

127

96

72

* 2 pints of PC were transfused that day

Laboratory Results Normal Range

Day 1

Day 2

Urea

1.7-8.3 mmol/L

11.1

10.8

Na

135-145 mmol/L

138

140

K

3.5-5.0 mmol/L

4.1

4.8

Ca

2.1-2.6 mmol/L

Mg

0.7-1.3 mmol/L

PO4-

0.8-1.45 mmol/L 64-122 umol/L

Scr

83

Day 3

Day 4

Laboratory Results Normal Range Albumin

35-50 g/L

T. < 20 umol/L Bilirubin

Day 1 29 27.9

T. Protein 66-87 g/L

64

ALP

53-141 u/L

88

ALT

< 32 u/L

56

Day 2

Day 3

Day 4

Laboratory Results Normal Range PT APTT INR

Day 1

10-13.5 sec

14.7

26-42 sec

37.1

< 1.5

1.35

Day 2

Day 3

Day 4

Laboratory Results

Normal Range CK

24-195 u/l

LDH

0-248 u/L

AST

<37

Day 1

60

Day 2

Day 3

Day 4

Daily Monitoring Normal Range BP

Day 1

Day 2

Day 3

Day 4

110/60

100/60

110/61

138/80

37 C

37

38

37

37

RR

12-18/ min

20

20

20

21

PR

60-100/min

86

94

62

70

Temp

Medication Dose

Frequency

D1 D2 D3 D4

Cardiovascular T. Propanolol

40 mg STAT, BD 1/52 Y

Y

Y

Y

Others IV Pantoprazole S/C Sandostatin

40 mg STAT, BD 1/52 Y 0.1 mg STAT, TDS 1/52

Y Y

Y Y

Y Y

(Octreotide)

Clinical Progress 

Day 1

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Passing black stool 2/7 a/w hematemesis once today

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No fresh blood, spitting black mouth/ blood.

−

No SOB, no chest pain, no diarrhea.

−

Abdomen discomfort and pain

−

OE: Alert and conscious

−

Sclera or conjunctiva no jaundice

−

Skin tugor good

−

CVS: DRNM

Plan −

Start IV 3 pint D5, 2 pint NS

−

ICNBN

−

For OGDS tomorrow

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Start IV pantoprazole 30 mg BD

−

T. Propanol 40 mg BD

Clinical Progress •

Day 2

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Plans:

–

Lethargy

−

OGDS today

–

PU normal

−

KNBM

–

has flatus

−

–

PR showed fresh malena

Cont. IV 2 pint NS and 3 pints D5

–

Refused CBD insertion

Clinical Progress 

Day 3

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Plan

−

BO with fresh malena

−

Cont KNBM

−

PU normal

−

Cont IVD 5 pint (2NS, 3 D5)

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Cont . 2 pack cell for transfusion

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Cont. v/s monitoring

Clinical Progress 

Day 4

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Plan

−

PU

−

Discharge today

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PR = fresh blood

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Syrup lactulose 30 mls ON

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T propanolol 40 mg BD

−

TCA 1/12 with rebanding

Discharge Medication 

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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 –

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Causes vasoconstriction, thus reducing splanchnic blood flow

TCA: –

1/12 with rebanding

–

OGDS on 7 December 2009

The End.... :D