GIT

د. حسين محمد جمعه

اختصاصي الامراض الباطنة
البورد العربي
كلية طب الموصل
2012

Upper Gastrointestinal Haemorrhage: a guide to diagnosis and emergency management

© 2011 BMJ Publishing Group Ltd

Evidence Based Review

1. Context
Commonest and most important gastroenterological emergency
25000 emergency admissions in UK p.a.
10-12% MR – mainly the elderly
Overall MR unchanged for > 20 years though age-related MR has reduced .


Commonly used terms
Haematemesis
Indicates GI haemorrhage proximal to ligament of Treitz
“Coffee ground” vomit
Altered blood from haemorrhage proximal to ligament of Treitz
Usually low or insignificant volume
Often associated with gastric stasis
Melaena
Haemorrhage (minimum 60 ml) from upper GI tract to proximal colon
Minimum 8 hours in GI tract to produce melaena

Haemochezia

Fresh blood per rectum due to lower GI or massive upper GI haemorrhage
Commonest Sites :
Duodenal Ulcer (DU) 25%
Gastric and duodenal erosions 25%
Gastric Ulcer (GU) 20%
Mallory-Weiss (MW) Syndrome 10-15%
Varices 5-10%
Oesophagitis 10


Rare causes :
Upper GI neoplasm
Aorto-enteric fistula
Angiodysplasia

2. Pathophysiology

i) 80% of upper GI haemorrhages stop spontaneously
ii) Clinical presentation depends on:
The rate of haemorrhage
The duration of haemorrhage
The patient's co-morbidities
iii) Mortality depends on:

• The rate of haemorrhage

• The duration of haemorrhage
• The site of haemorrhage: Varices (MR 30%), PU (MR 10%) and MW syndrome (MR < 1%)
• The patient's co-morbidities (often reflected in the age of the patient) 2% MR up to age 60, and Steep rise in MR above 60
• Death is rarely due to exsanguination and instead occurs due to decompensation of co-morbid conditions
iii) Mortality depends on:

a) Peptic Ulcer disease

Acute haemorrhage due to erosion into artery
Lesser curve GU – branches of left gastric artery
Posterior DU – gastro-duodenal artery complex
DU are usually acute events and rarely present with iron deficiency anaemia
Often little history of dyspepsia
Usual cause is Helicobacter pylori (HP) infection or NSAID use.


The proportion varies with population infection rates and drug use.
2% of PU will have neither risk factor: usually related to severe physiological stress - Burns (Curlings ulcer); CNS disease (Cushings ulcer); SIRS
Corticosteroids do not cause PU but potentiate the risk with HP infection or NSAID use
80% stop bleeding spontaneously

b) Gastric erosions

Associated with alcohol, NSAIDS and severe physiological stress
c) MW Syndrome
Oesophago-gastric mucosal tears preceded by retching or vomiting that is followed by haematemesis
d) Varices
Varices have a MR of up to 50%. The aetiology and management differ significantly from other causes of upper GI haemorrhage.
See separate learning module

3. Assessment

a) Estimate blood loss
Clinical presentation varies with patients co-morbidities and ability to compensate for losses
In acute haemorrhage the haematocrit level should decrease but the value may not be correlated with real blood loss because of haemodilution and equilibration with extravascular fluid .

b) Confirm the source of haemorrhage is upper GI. The presence of haematemesis indicates bleeding proximal to ligament of Treitz. Melaena without haematemesis or massive haematochezia may require nasogastric (NG) tube aspiration to help determine the source of haemorrhage.
c) Consider if the source of haemorrhage is variceal. Take an alcohol history. Search for stigmata of chronic liver disease and the presence and severity of hepatic encephalopathy. Treat any patient with a high index of suspicion for variceal haemorrhage as variceal haemorrhage until proven otherwise.


d) Historical features such as epigastric pain, nausea, vomiting, anorexia, weight loss and drug use do not help to differentiate cause or focus management
e)Essential investigations are:
Renal and liver profile
Full blood count
Cross-match
Consider coagulation screen and ECG

4.Therapeutic Interventions

a)Initial Resuscitation
Oxygen and airway intervention as required
IV access and volume replacement with crystalloid and blood
Central venous pressure monitoring to guide fluid replacement if severe haemorrhage, significant co-morbidities or failure of shock to respond to initial fluid resuscitation
No evidence for hypotensive resuscitation in GI haemorrhage and unlikely to helpful as : 80% stop spontaneously and Death is rarely due to exsanguination
Correct coagulation abnormalities

b)Acid Suppression

i) Theoretical benefit as when pH < 6 this:
Compromises the coagulation cascade
Prevents platelet aggregation
Causes platelet disaggregation
Increases pepsin activity (maximal at pH 2, minimal > pH 5) which promotes clot lysis


ii) H2 receptor antagonists
Do not reliably raise pH above 6
Patients develop tolerance
Cochrane review of H2RA in acute peptic ulcer bleeding (2004) – no overall effect on mortality, rebleed or surgical intervention rate

iii) Proton pump inhibitors (PPI)

Lau et al 2000 – trial of PPI Hong Kong
80mg IV then 8mg/hr for 72 hours post therapeutic endoscopy
Intragastric pH > 7 within 20 minutes
Re-bleed rate 6.7% vs. 22.5% (placebo)
Surgical intervention 3% vs. 9% (placebo)
BUT: Post OGD so benefit in emergency use unclear

PPI treatment initiated prior to endoscopic diagnosis - Cochrane Review July 2006

5 RCT with 1512 patients
Significant reduction in proportion of patients with stigmata of recent haemorrhage at index endoscopy
No evidence of benefit on clinically important outcomes – MR, re-bleeding or surgical intervention rate.
Highly heterogeneous trial results noted. Heterogeneity resolved by separating trials into 2 groups:

Non-Asian Patients – no effect

Asian patients – significant effect
Significant differences between Asian and non-Asian patient groups:
Low co-morbidity rate in Asian trial population
Low NSAID use in Asian trial population
Lower parietal cell mass in Asian population
Omeprazole more effective in Asian population due to cytochrome defect which produces a prolonged effect.


Lau JY et al 2007 - trial of PPI Hong Kong
80mg IV then 8mg/hr before therapeutic OGD the next morning in a largely Asian population
Significant reduction in:
Proportion of patients with stigmata of recent haemorrhage at index endoscopy
Proportion of patients with active haemorrhage at index endoscopy
Proportion of patients requiring treatment at index endoscopy .
BUT No significant difference:
Mean blood transfusion requirement
Rate of recurrent bleeding
Risk of emergency surgery
30 day MR

c) Vasoconstrictors

Somatostatin and Terlipressin inhibit gastric acid secretion, pancreatic secretion and biliary secretion. They also reduce gastric mucosal blood flow, gastric perfusion and stimulate mucus production. The increase in pH theoretically allows optimum platelet function and decreases fibrinolysis. An evidence based review[5] suggests a beneficial effect for somatostatin in upper GI haemorrhage secondary to probable peptic ulcer for acute, severe upper GI haemorrhage pending therapeutic endoscopy.

BSG guidelines 2002[6] suggest there remains insufficient evidence as the individual trials included in the main meta-analysis were of such poor quality. Consensus guidelines from 2003 [7] suggest consideration of somatostatin in life-threatening haemorrhage.
Despite the theoretical benefit of Terlipressin there are no published studies on its use in non-variceal haemorrhage
Octreotide has no evidence to support its use[8]

d) Diagnostic OGD

No reduction in MR
No reduction in hospital stay
No reduction in transfusion
Identifies precise site in 90%


e) Diagnostic +/- therapeutic OGD
Endoscopy is a critical early intervention that can be used to establish the source of bleeding, and it also offers therapeutic options.
Haemostasis is achieved by injection of various agents, the application of heat or mechanical clips
75% reduction in re-bleeding and referral for surgery
40% reduction in MR
Endoscopy is recommended within 24 hours of admission with facilities for emergency endoscopy available on a 24 hour basis .

f) Management of Re-bleeding

Re-bleeding is haematemesis and/or melaena associated with the development of shock, CVP fall > 5 cm H2O or a reduction of haemoglobin > 20g/l over 24 hours
Re-bleeding is associated with 10 times increased MR
Re-bleeding is associated with: Atheroma – vessels unable to contract effectively
Posterior wall DU
High lesser curve GU
Vessel visible in ulcer base.

If re-bleed occurs after initial period of clinical stability therapeutic endoscopy is the first management step even if there has been a previous therapeutic endoscopy.[6] Lau JYW et al demonstrated at least as good a prognosis compared to emergency surgery for this approach[9]
Emergency surgery has a reported MR of between 10 and 50%. It is reserved for uncontrollable haemorrhage. However, surgical criteria for intervention are variable and depend on local resources.

5. Risk Stratification

Approximately 80% of patients will stop bleeding spontaneously without recurrence
Most morbidity and mortality occurs among the remaining 20% who have continued or recurrent bleeding
The main goal of management is to identify patients at high risk for an adverse outcome on the basis of clinical or laboratory variables
Identification of low risk patients is also possible which may prevent in-patient admission and emergency endoscopy.


a) Rockall Score
Developed 1996 from a prospective population study with prospective revalidation in a second population group
Externally validated in a number of countries
Derived from 5 variables: age, presence of shock, co-morbidities, endoscopic diagnosis and endoscopic macroscopic findings.

Predicts re-bleeding and re-bleeding mortality

Identifies 26% of cases after OGD with low risk of re-bleed and low MR (Score < 3)
Identifies 13% of cases after OGD with low risk of re-bleed and zero MR (Score < 2)
Reliance on endoscopic findings means its utility in emergency practice is limited.

b) Clinical Rockall Score

Developed from the Rockall score
Derived from the 3 clinical variables with a maximum score of 7
Despite its widespread use it has not been prospectively validated
Gralnek and Dulai [12] retrospectively compared the clinical and complete Rockall Score for 175 patients.

The clinical Rockall Score identified 12% as at low risk of death (score 0) and none of these had a re-bleed
The complete Rockall Score identified 30% as at low risk of death though 3.8% did re-bleed (without dieing)
No patient identified as low risk for death by the clinical Rockall Score was not low risk on the complete score
No patient identified as low risk for death by the clinical Rockall Score had a re-bleed .


Tham, James and Kelly retrospectively compared Rockall scores in 102 cases. They confirmed that a low clinical Rockall Score identified a group of patients with no risk of re-bleed or death.
Therefore the clinical Rockall Score appears to effectively identify both those patients at low risk of death and re-bleeding and those who do not require urgent clinical intervention. However it has not been prospectively validated.

c) Glasgow Admission (Blatchford) Score

A non-endoscopic risk score developed by Blatchford O et al.
Developed 2000 from a retrospective population study with prospective validation in a second population group
A number of variables are scored
A score of < 2 identifies both those patients at low risk of death and re-bleeding and those who do not require urgent clinical intervention allowing for discharge from the Emergency Department and out-patient management of the upper GI haemorrhage (Sensitivity 99%)

The Blatchford score is often used sequentially with the complete Rockall score, the first to identify patients at low risk who can be discharged , the second to identify those among the admitted patients at high risk of re-bleed and death.
However, a recent study comparing the Blatchford, complete Rockall and clinical Rockall Scores in emergency identification of high risk patients was published in 2007. [15] All patients who presented with upper GI haemorrhage who required any clinical intervention were identified and scored.

The Blatchford Score was most specific identifying 245 of 246 patients as high risk, compared to 222 with a clinical Rockall Score of > 0 and 224 with a complete Rockall Score of >2. This suggests the Blatchford score could be used alone to identify both low and high risk patients though to complicate matters the researchers used a Blatchford score cut-off of > 0 rather than the standard > 1.

Score:

0
1
2
3
Age:
< 60
60-80
> 80


Shock:
None
Tachycardia
Hypotension

Co-morbidity:

None

CCF / IHD

Renal failure. Liver failure. Malignancy.
Diagnosis:
No lesion. MW tear
No lesion. MW tear
Malignancy

OGD:

Black spots

Blood in lumen. Adherent clot. Visible vessel. Bleeding vessel

• Upper Gastrointestinal Haemorrhage: a guide to diagnosis and emergency management
• Rockall Score


Risk Score
Predicted Re-bleed (%)
Predicted MR (%)
0
5
0
1
3
0
2
5
0
3
11
3
4
14
5
5
24
11
6
33
17
7
44
27
8+
42
41
• Upper Gastrointestinal Haemorrhage: a guide to diagnosis and emergency management
• Rockall Score


Admission Risk
Score
Urea

>6.5-<8.0

2
>8.0-<10
3
>10-<25
4
> 25
5
Haemoglobin (men)

>12-<13

1
>10-<12
3
< 10
6
Haemoglobin (women)


>10-<12
1
< 10
6
Systolic BP

100-109

1
90-99
2
< 90
3
Other Markers

Pulse > 100

1
Melaena
1
Syncope
1
Hepatic Disease
2
Cardiac failure
2


All other parameters score 0

Score < 2 = home / routine OPD OGD

• Glasgow Admission (Blatchford) Score

Upper gastrointestinal bleeding: a guide to diagnosis and management of non-variceal bleeding

Key points

You should immediately assess the volume of blood loss in all patients who you suspect have an upper gastrointestinal bleed, before proceeding to a more thorough history and examination.
You should aim to restore the circulating blood volume as soon as possible.
When you have stabilised the patient, you should organise an endoscopy.
Most patients should have an endoscopy within the first 24 hours after they have been resuscitated and their condition has stabilised.

Clinical tips

If it is obvious that there is a large amount of blood loss, ask the blood bank to supply four units of cross-matched blood as soon as possible
You should make the endoscopy and surgical teams aware at an early stage of any patients who appear to have had a large upper gastrointestinal bleed
Give instructions to the nursing staff on how to detect rebleeding. Make it clear what changes in heart rate, blood pressure, and central venous pressure should make them contact a doctor.

Introduction

Acute gastrointestinal bleeding is the most common gastrointestinal emergency. The incidence is 50 to 150 cases per 100 000 of the adult population, and it leads to 35 000 hospital admissions per year in the United Kingdom.1
Despite the advent of endoscopy and advances in drug treatment and the care of critically ill patients, the overall mortality of patients admitted to hospital with upper gastrointestinal bleeding has not changed in the past 50 years.


Rockall reports an 11% mortality in patients admitted to hospital with a primary diagnosis of upper gastrointestinal bleed, and a 33% mortality in patients who develop upper gastrointestinal bleeding while an inpatient.

The explanation for the unchanging mortality lies in the changing population of those presenting with upper gastrointestinal bleeding. Half of all patients admitted to hospital with upper gastrointestinal bleeding are now over 60 years old. Because patients who present with an upper gastrointestinal bleed nowadays are older and also have greater comorbidities than patients who presented with upper gastrointestinal bleeds in the past, their mortality is inherently higher than it was 50 years ago.

The mortality in patients who develop upper gastrointestinal bleeding while already in hospital is threefold more than those who are admitted from the community.1
There is some evidence that concentrating the care of patients with upper gastrointestinal bleeding into a defined specialist area can reduce mortality.

Table 1: Common causes of acute upper gastrointestinal haemorrhage3

Diagnosis
Approximate % of total
Peptic ulcer
35-50
Gastric and duodenal erosions
8-15
Oesophagitis
5-15
Mallory-Weiss syndrome
15
Oesophageal varices
5-10
Upper gastrointestinal malignancy
1
Vascular malformations
5
Rare
5
• Causes of upper gastrointestinal bleeding


Notes on table 1
Duodenal ulcers are more prevalent in areas with relatively low socioeconomic status, which reflects the high prevalence of Helicobacter pylori in this group.4
A careful drug history, including questions about over the counter medications, is essential. Erosive gastritis and duodenitis may result from drugs such as aspirin and non-steroidal anti-inflammatory drugs, some of which can be obtained without prescription.
The incidence of reflux oesophagitis has increased over the past 25 years for reasons that remain unclear.

In Mallory-Weiss syndrome, the bleeding that results from the linear tear at the oesophagogastric junction may resolve spontaneously without the need for endoscopy.
Although oesophageal varices account for less than 10% of episodes, mortality during the acute episode is about 30%.

Less common causes of upper gastrointestinal bleeding include:

Coagulation disorders and anticoagulation, for example, thrombocytopenia and warfarin. It is always important to consider whether the patient might have a clotting disorder. The risk of warfarin is well known, but the combination of aspirin and clopidogrel is one that is increasingly being used in interventional cardiology and is becoming an important cause of haemorrhage.

While it is usually appropriate to stop a drug that might be contributing to bleeding, it is also important to consider the original indication for the prescription and the possible risk to the patient if the drug is stopped.

Benign tumours, for example, leiomyoma. Gastrointestinal bleeding from benign tumours is less common than bleeding from malignant tumours
Dieulafoy's lesion. This is a vascular abnormality, recognised at endoscopy, where the artery fails to narrow as it reaches the mucosal surface. It can be difficult to identify during endoscopy unless it is actively bleeding during the procedure. If it is not identified at the initial endoscopy, further gastrointestinal bleeding may occur. At repeat endoscopy, it may be possible to identify an actively bleeding lesion

How gastrointestinal bleeding presents

Patients most commonly present with either haematemesis or melaena.
Vomited blood may appear fresh or look like coffee grounds. Melaena stools are black and tarry, and they have a memorable odour.

You may assume that patients who present with both haematemesis and melaena have rapid bleeding. The mortality of such patients is double that of those who present with either condition on its own.7 Usually, blood is partly digested in its passage through the gastrointestinal tract.
This accounts for the appearance of melaena. In massive upper gastrointestinal bleeding, however, red blood is occasionally passed rectally.


Clinical assessment
You should first assess the severity of the blood loss, and then you should focus on the likely cause of the bleeding. You should make an assessment of:
The volume of blood loss
The site of the bleeding
The general health of the patient.

Assessment of blood loss

Patients’ accounts of the severity of blood loss are notoriously unreliable. For most patients, the event is alarming and the tendency to exaggerate is understandable. The clinical assessment of the volume of blood loss may also be difficult and can often be inaccurate. It is essential that you assess the patient’s heart rate, blood pressure, peripheral perfusion, and conscious level. While specific values are arbitrary, a systolic blood pressure of less than 100 mm Hg and a heart rate of more than 100 beats per minute indicate that the volume of blood loss is likely to be large.

You should be aware that a postural drop in systolic blood pressure of more than 20 mm Hg on standing is an early indicator of loss of blood volume, and will occur before the patient becomes hypotensive.

Immediate resuscitation after assessment of blood loss

Check the airway (A), breathing (B), and then focus on the circulation (C). You need to:
Check the following blood tests:
Haemoglobin, white cell count, platelet count
Urea and electrolytes
Liver function tests
Prothrombin time
Blood group

Arrange a chest x ray and an ECG in high risk patients (those with a known cardiovascular and respiratory comorbidity)
Insert two large bore intravenous cannulae (size 14 or 18 gauge) into veins of sufficient calibre to allow a rapid infusion
Start intravenous fluids. Give either:
Crystalloid, for example, normal saline
Colloid, for example, Gelofusine.


Although there is no evidence to support one type of fluid over another, colloids have the advantage of producing faster and greater expansion of the intravascular volume than crystalloids.8 9 Consequently, clinicians tend to choose colloids while they wait for the cross-matched blood. Synthetic colloid or crystalloid will cause haemodilution.

Giving blood early in resuscitation is important in patients with signs of systemic shock (low blood pressure, tachycardia, altered consciousness) or overt continuous bleeding
The haemoglobin level on the initial full blood count can be misleading as an indicator of the severity of the bleed. Because haemoglobin is expressed as a concentration, its value will only begin to fall when the circulating volume is restored.

If the patient is in extremis, you should ask the blood bank for group O Rh negative blood

You should give blood up to a haemoglobin level of 10 g/dl
You must monitor the patient's heart rate and blood pressure continuously. You should consider inserting a central line in all patients who show signs of haemodynamic compromise. A central venous pressure:
Provides a more accurate guide to volume depletion
Can guide fluid replacement
Can prevent excessive fluid replacement, particularly in elderly people and in those with a comorbid disease

Insert a urinary catheter in all patients who need a central line.

The volume of urine produced is a guide to tissue perfusion. It should exceed 0.5 ml/kg per hour.
You should correct any coagulopathy, with the aim of correcting the INR to as near normal as possible
You should give additional fresh frozen plasma to patients receiving a transfusion of more than four units of blood, as the transfused blood does not contain clotting factors.
Keep the patient nil by mouth until endoscopy.

Assessment of the site of the bleeding

You should consider what might be the site of the bleeding only when resuscitation is underway. When taking a history, you should focus on symptoms that might be associated with the various causes. Ask about:
A history of dyspepsia
Drug history - many patients do not necessarily regard aspirin and aspirin containing medications as drugs.
A history of repeated vomiting - repeated vomiting before the blood appears suggests a Mallory-Weiss tear.
A history of chronic liver disease - this might suggest oesophageal varices as a possible cause.


Clinical examination is most helpful for assessing the severity of the blood loss. It rarely helps identify the cause. Occasionally, patients will have an epigastric mass or lymphadenopathy suggesting malignancy. Spider naevi, leuconychia, palmar erythema, and gynaecomastia suggest chronic liver disease. In the presence of possible liver disease, splenomegaly indicates that portal hypertension is likely, which should make you think about oesophageal varices.

Assessment of the general health of the patient

The presence of comorbid disease such as a cardiac or respiratory disease is important for the risk assessment, which is an important guide to the management of gastrointestinal bleeding.

Table 2: Rockall score1

Variable
Score

0
1
2
3
Age
<60 years
60 to 79 years
>79 years

Shock

Pulse <100
Systolic BP >100 mm Hg
Pulse >100
Systolic BP >100 mm Hg
Pulse >100
Systolic BP <100 mm Hg


Comorbidity
None

Cardiac disease

Any other major comorbidity
Renal failure
Liver failure
Disseminated malignancy
Endoscopic diagnosis
Mallory-Weiss tear, no lesion
All other diagnoses
Malignancy of the upper gastrointestinal tract

Major stigmata of recent haemorrhage

None or dark spots

Blood in the upper gastrointestinal tract, adherent clot, or spurting vessel

• Risk assessment in gastrointestinal bleeding
• Because of the high mortality, scoring systems have been developed to identify those patients who are at high risk of adverse outcomes following acute upper gastrointestinal bleeding. The most commonly used scoring system is that devised by Rockall and colleagues (tables 2 and 3).


Rockall score
This was devised from a prospective audit of over 40 000 patients presenting with upper gastrointestinal bleeding. Rockall and his colleagues defined a series of risk factors which independently predict mortality.1
Age
Death from upper gastrointestinal bleeding is rare under the age of 50 years, but increases thereafter so that the mortality rate at the age of 90 years is 30%.
Shock
The risk progressively increases as the heart rate rises and the blood pressure subsequently falls.

Comorbidity

The risk of dying is greatly increased if the patient also has a chronic medical disease. The likelihood of death is greatest in patients with advanced liver and renal failure, and in those with metastatic cancer.

Findings at endoscopy

The last constituent of the Rockall score are the findings at endoscopy. Two scores are calculated; the initial pre-endoscopy score and the post-endoscopy score. Patients with an initial score of:
Less than or equal to 2 should be observed and treated medically. You should arrange an outpatient endoscopy within one week.
More than 2 and less than or equal to 4 should have an endoscopy as an inpatient the following day
More than or equal to 4 have a high risk of further bleeding. Such patients should be endoscoped by an experienced therapeutic endoscopist as soon as they have been resuscitated.

Table 3: Rebleed and mortality risk according to Rockall score1

Risk score
Predicted mortality pre-endoscopy (%)
Predicted rebleed risk (%)
Predicted mortality post-endoscopy (%)
0
0.2
5
0.0
1
2.4
3
0.0
2
5.6
5
0.2
3
11.0
11
2.9
4
24.6
14
5.3
5
39.6
24
10.8
6
48.9
33
17.3
7
50.0
44
27.0
8+


42
41.1

Endoscopy

Endoscopy has changed from being just a diagnostic tool to becoming a therapeutic tool as well. This has led to a reduction in emergency surgery.10 Because endoscopy may be needed urgently, it has been recommended that all acute hospitals provide 24 hour cover for emergency endoscopy.3 Such a service is not currently universally available.

Endoscopy in acute upper gastrointestinal bleeding is used to:

Determine the cause of the bleeding
Stratify the risk of the patient rebleeding
Treat lesions.

Endoscopy can be performed either as an urgent or as a semi-elective procedure, depending on the clinical circumstances. You must ensure that you have adequately resuscitated the patient prior to endoscopy. This is not always possible when the haemorrhage is very heavy or rapid. In this situation, you should arrange for an urgent endoscopy in a specialised environment such as an operating theatre.

You should only arrange for a routine repeat endoscopy six weeks later in patients with a bleeding gastric or oesophageal ulcer, in order that biopsies can be taken from the ulcer base and edges to exclude malignancy.

Endoscopy

The endoscopic appearance of a bleeding peptic ulcer can take five different forms.11 The endoscopist should make a decision regarding interventional treatment based on the appearance of the ulcer. This is because the appearance of the ulcer has been shown to be associated with the risk of bleeding on medical management (the percentage of risk involved is shown in parentheses).12
A clean based ulcer (3% to 5%)
A flat spot (7% to 10%)
Generalised oozing without visible vessel (10% to 20%)
An adherent clot on the ulcer surface (25% to 30%)
A non-bleeding vessel (50%)
Active ulcer bleeding (90%).


Endoscopic treatments
Patients with clean based ulcers do not need any intervention.
Patients with a non-bleeding visible vessel or an active arterial bleed should be treated endoscopically to achieve haemostasis. Combination therapy is superior to monotherapy in reducing the rate of rebleeding and the need for surgery.13 Combination therapy describes injection therapy (adrenaline, fibrin glue) in combination with:
Thermal therapy (heater probe, argon plasma coagulator)
Mechanical clipping

It is important that an experienced endoscopist, who is familiar with the intervention being used, performs endoscopic intervention.
Patients with ulcers with adherent clots should be treated by clot removal, followed by endoscopic treatment of the lesion that lies beneath the clot. This has been shown to decrease the rate of recurrent bleeding.14
Patients with Mallory-Weiss tears tend to stop bleeding spontaneously.

Occasionally, injection or thermal therapy may be necessary to achieve haemostasis. Other causes of bleeding, such as vascular ectasias, flat spots with oozing without a visible vessel, and erosions, can be treated with thermal therapy.
Brush cytology can be taken safely at emergency endoscopy in cases where you suspect that a malignant ulcer is the cause of the patient's bleeding. But it is best to arrange a further endoscopy after the bleeding has stopped, so that biopsies can be taken.

Rebleeding

Despite treatment at endoscopy, rebleeding may still occur in as many as 20% of patients.
In a study of 3386 patients with bleeding from an ulcer, independent predictors of rebleeding were15:
Hypotension
Fresh blood
Haemoglobin less than 10 g/dl
Ulcer diameter of more than 2 cm
Active bleeding.


You should give instructions to the nursing staff on how to detect rebleeding. Make it clear what changes in heart rate, blood pressure, and central venous pressure should make them contact a doctor.
In episodes of recurrent bleeding from peptic ulcers, you should consider arranging a repeat endoscopy. A repeat endoscopy decreases the need for surgery, does not increase mortality, and has fewer complications than surgery.

Pharmacological treatments

Acid suppression
The use of acid suppressing drugs following gastrointestinal haemorrhage is supported by the evidence that an intragastric pH below 5 promotes clot dissolution, whereas a pH above 6 promotes platelet aggregation and clot formation. Treatment with intravenous proton pump inhibitors (PPIs) is beneficial in upper gastrointestinal bleeding secondary to peptic ulcer disease.

Although a recent study suggested that giving high dose intravenous omeprazole early to patients with upper gastrointestinal bleeding, before endoscopy, significantly reduces ulcer bleeding,18 there is currently no evidence for the empirical use of intravenous omeprazole prior to endoscopy in patients with suspected upper gastrointestinal bleeding.

Current recommendations, based on a landmark randomised, double blind, placebo controlled study, are19:
You should only give intravenous proton pump inhibitors to patients with bleeding peptic ulcer disease after endoscopic haemostasis. You should give a high dose 80 mg bolus, followed by an infusion at a rate of 8 mg per hour for up to 72 hours. This has been shown to reduce the rate of rebleeding following peptic ulcer bleeding, but the need for surgery and the 30 day mortality are not altered.

In patients with active upper gastrointestinal bleeding, where blood loss has resulted in signs of a fall in cardiac output, you can give proton pump inhibitors by intravenous bolus (80 mg once daily) while the patient is awaiting endoscopy. You should stop treatment as soon as patients can tolerate an oral proton pump inhibitor.

All patients should complete eight weeks of treatment with a proton pump inhibitor. Patients who are on regular low dose aspirin or who are using non-steroidal anti-inflammatory drugs and cannot stop them, appear to be at high risk of developing recurrent ulcers. Such patients may benefit from maintenance treatment with proton pump inhibitors.20

Eradication treatment for Helicobacter pylori

The presence of H pylori has been shown to increase the risk of rebleeding in patients with peptic ulcer disease.21 All patients with bleeding from peptic ulcer disease should be tested at the time of emergency endoscopy. You should give eradication treatment to positive patients as soon as oral feeding is restarted. It is important to confirm that eradication of H pylori has been successful after an ulcer has bled. This is best done by an isotope test three months after treatment.

Surgery

You should inform the on call surgical team at an early stage of all high risk patients (initial Rockall score equal to or greater than 3) in whom there is the potential for surgical intervention. Delay increases mortality in these patients. You should consider surgery if:
• The bleeding persists
• Rebleeding occurs after two therapeutic endoscopies.


Before deciding whether to proceed to surgery, you need to consider the patient's age, comorbidity, ulcer size, and estimate the likely volume of blood transfusion needed for all patients. Patients with ulcers larger than 2 cm are more likely to fail repeat endoscopic treatment and require surgery.
Older patients and those with important comorbid diseases, who poorly tolerate prolonged resuscitation, large volume transfusions, and periods of hypotension, have a lower threshold for surgery.

Approach to a patient with an unclear source of upper gastrointestinal bleeding

This is a common problem, occurring in up to 20% of patients with acute upper gastrointestinal bleeding.11 You should arrange for a repeat endoscopy if the predicted mortality is above 10%. If a good view of the upper gastrointestinal tract is achieved during endoscopy, but no definite cause of the bleeding is found, the rest of the small bowel should be examined. This can be done endoscopically (capsule endoscopy or push enteroscopy) or radiologically (small bowel follow through). Of these imaging tests, capsule endoscopy has been shown to be the investigation of choice.

Death is rarely due to exsanguination and instead occurs due to decompensation of co-morbid conditions .
The clinical Rockall Score appears to effectively identify both those patients at low risk of death and re-bleeding and those who do not require urgent clinical intervention but it is less specific and sensitive than the complete score.
The complete Rockall score identifies about 30% of patients with MR of 0% and a re-bleed rate of < 4%.

The Rockall score identifies only about a third of these patients. 2% MR up to age 60 then a steep rise in MR above 60.
Variceal haemorrhage has an overall MR of up to 50% compared to the 10-12% for upper GI haemorrhage.
Peptic ulcers account for almost 50% of all upper GI haemorrhages .
The risk of rebleeding on medical management for an adherent clot is 25% to 30%. A routine repeat endoscopy is only necessary for oesophageal and gastric ulcers.