Management of bleeding peptic ulcer..ppt

peptic ulcer disease management

1. Management of bleeding peptic ulcer:
Introduction
•Upper gastric bleeding remains the most common
gastrointestinal emergency. A recent audial by the BSG
found an overall incidence of 100 per 100,000
adults/annum, which has not changed much over the last
30 – 40 years.
•Bleeding occurs in 15 – 20% of patients with PUD, it is
more common in those more than 60 yrs due to
increased use of NSAIDS. Up to 20% bleed without any
prior warning, signs or symptoms.

2. Presentation
•Slow Bleeders
- Aneamia
- Melaena stools
•Rapid bleeders
- Haematamesis
- Malaena stools
- Haematochezia
- Anaemia
- Cardiovascular symptoms

3. Cardiovascular Response to G. Bleeding loss not exceeding
20% of blood volume:
• About 10% of total blood volume can be lost without significant effect on arterial
blood pressure or cardiac output. Further loss results in progressive reduction in
both; after loss of 35 – 40% cardiac output falls to near zero.
• In the observe of tissue injury low levels of acute blood loss lead to
compensatory mechanism.
• Increase in heart rate
• Increase in systemic vascular resistance
• Reduce spanchnic neck blood flow.
• Reduce blood flow through:-
1) Splanchous circulation
2) Muscles
3) Skin
4) Venous reservous constrict
• These CVS charges are triggered by decreased vagotone and increased
sympathetic activity and are mediated by the Baroseflex, the sensitivity is
increased by haemorrhage.

4. As blood loss increases, the following happens:-
•Increase in vago tone leading to slowing of the heart rate.
•Fall in blood pressure due to decreased systemic vascular resistance.
•Syncope.
As blood loss increases above 30% of blood volume, the following happens:-
•Heart rate may again rise simple measures of vital signs may be for indicator of blood
loss.
•Decreased blood flow through the aortic and carotic bodies activates chemoreception
that do the following.
•Vagally mediated brady cardia.
•Sympathetically mediated vasoconstriction and increased respiration.
•The tachy cardia reduces the reflex brady cardia mediated by cardiac c-fibre efferents
and therefore during the hypotensive phase following severe haemorrhage, stimulation
of arterial chemoreceptors may prevent further falls in the blood pressure.
•During severe hyporolaemia flow through the brain and heart are preserved.
•Increased sympathetic activity does not cause significant coronay and cerebral vascular
spasm.
•Autoregulation of blood flow predominates when blood flow continues and falls to very
low levels, reduced coronay blood flow will lead to decreased cardiac output and
ultimately death.
Loss Exceeding 20% of blood
volume:

5. Evaluation of blood loss:-
•Initial step include:
–vital signs
–Pulse
–Blood pressure
–Postural changes in pulse and Blood pressure

6. Bleeding History:
•Coffee ground, haematemesis
•Melaenia stools
•Red haematemesis and melaence occurring
together 50 – 100ml of blood is sufficient to
cause melaema
•Haemotochaesia often associated with
hyporolaemia

7. Stomach Contents
•Best avoided. Nasogastric aspiration does
not help to show the site of bleeding.

8. Vital signs
Not useful in isolation may not give an accurate reflection of blood loss.
May be influenced by the following:
•Age
•Concurrent illness like DM.
•Drug intake
Significant blood loss
•Pulse rate > 100/min
•Systolic BP of < 100mml
•Drop in diasiolic pressure more than 10 mm on standing or sitting
•Pallor
•Sweating
•Shock index (PR/SBP) Better
• <25% blood loss give shock index <1.0
•25% - 33% - 1.0
•>33%, blood loss – shock index >1

9. Central Venous Pressure
•Acute blood loss decreases venous return
causing a fall in CVP. Blood loss correlates well
with CVP.

10. Haemotocrit
•Useful after 72 hrs as loss of blood involves
whole blood.
•How much blood has been lost?
•Initial assessment of blood loss depends on a
combination of the history and regular recording
of pulse, blood pressure and postural changes in
blood pressure and pulse.
•Volume deficit is well reflected by the shock
index (pulse/rate/SBP)

11. Signs of significant blood loss
•Pulse > 100/min
•SBP < 100 mmHg
•Diastolic BP drop on sitting or standing
>10mmHg
•Pallor and sweating
•Shock index > 1

12. Assessment of patients Risk high risk
•Advanced age > 60 yrs
•Presence of serious comorbid states
•Signs of hypovolaemia
•Health patients under age of 60 yrs of age with no other illness have
a mortality rate 2.3% mortality in those at increased risk goes up 2-4
times higher
Presence of hypovolaemia
•Systolic BP < 100mmHg
•Diastolic blood pressure falls on sitting/standing by > 10 mmHg
•Pulse > 100bpm
•Shock index > 1

13. Assessment of patients at high risk. Cont
Haemoglobin on presentation
•< 10g/dl
Presence of severe concomitant disease
•Cardiovascular
•Respiratory
•Renal
•Hepatic
Symptoms of GIT Bleed
•Bright red blood in vomits and stool

14. High risk ulcer
•Arterial spurting
•Oozing of blood
•Non bleeding visible vessel
•Adherent clot
•Each has a specific risk for adverse out come.
Risk of re-bleeding approximates
•90% for arterial bleeding
•50% non bleeding visible vessel
•12 – 33% adhered clot
•18 – 27% for oozing

15. Physical Examination
Main aims
•Evaluate respiratory systems
•Haemodynamic status
•Postural hypertension
Do complete resuscitation then complete PE
•Jaundice
•Spider naïve
•Liver asterexis
•Hepatosplenomegaly
•Crest syndrome
•High risk patients – admit to HDU

16. Initial management
Presentation with Acute/GTI Bleed
ABC of Resuscitation – secure airways
Assessment for high risk factors .
History, examination, blood tests
High risk Low risk

17. High risk
IV Access
2 lines ±
CVP
Monitor
Hyporolaemia
Urinary Catheter
Oxygen
Fluid replacement
Correct cloting disorders
Normovalaemia
Admit to HDU
Urgent Endoscopy

18. Low risk
IV Access
Admit to general ward
Elective endoscopy

19. Treatment for Bleeding Peptic Ulcers
Pharmacotherapy
• Pharmacotherapy may influence the outcome of peptic ulcer
bleeding in three ways
• Reduction of gastric acid production this producing more
favourable environment for peptic ulcer healing and clot
formation.
• Reducing fibrinolysis at ulcer site
• Reducing splanchnic blood flow
Best acid suppressive regimen
• 80 mg pantoprazole/omepazole bolus followed by 8mg.hr
infusion until bleeding stops.
Acid inhibiting Drugs
• Enhance peptic ulcer healing
• Expedite clot formation and keeps clot stable
• Reducing re-bleeding

20. Treatment for Bleeding Peptic Ulcers
•Antifibrinoytic agents
•Inhibit plasminogen activation by activators found in
gastric and duodenal mucosae and by pepsin.
•40% reduction in mortality 20 –35% reduction in re-
bleeding
•30 – 40% reduction in need for surgery
•Somatostatin and Octreotide
•Reduce splanchnic blood flow
•Inhibit output of gastric acid, pepsin and gastrin
•Benefits doubtful
•Endotherapy
•Surgery