Presenting problems in gastrointestinal disease  797

vomiting from regurgitation and to elicit whether the vomiting is acute

Dyspepsia
or chronic (recurrent), as the underlying causes may differ. The major
causes are shown in Figure 23.18.
Are there
'alarm' features? Gastrointestinal bleeding
Yes No
Acute upper gastrointestinal bleeding
< 55 years > 55 years This is the most common gastrointestinal emergency, with an estimated
incidence of 134 per 100 000 of the population in the UK; the mortality of
Urgent Endoscopy patients admitted to hospital is around 10%. Risk scoring systems have
endoscopy been developed to stratify the risk of needing endoscopic therapy or of
having a poor outcome (Box 23.16). The advantage of the Blatchford
Test for Helicobacter pylori, e.g. serology, score is that it may be used before endoscopy to predict the need for
stool antigen or 13C urea breath test
intervention to treat bleeding. Low scores (2 or less) are associated with
a very low risk of adverse outcome. The common causes are shown in
Figure 23.19.
Positive Negative
Clinical assessment
Haematemesis is red with clots when bleeding is rapid and profuse,
Helicobacter pylori Treat
eradication symptomatically or black (‘coffee grounds’) when less severe. Syncope may occur
or and is caused by hypotension from intravascular volume depletion.
consider other Symptoms of anaemia suggest chronic bleeding. Melaena is the
diagnoses
passage of black, tarry stools containing altered blood; it is usually
Symptoms Symptoms
resolve persist caused by bleeding from the upper gastrointestinal tract, although
haemorrhage from the right side of the colon is occasionally respon-
No sible. The characteristic colour and smell are the result of the action
follow-up Endoscopy of digestive enzymes and of bacteria on haemoglobin. Severe acute
upper gastrointestinal bleeding can sometimes cause maroon or
Fig. 23.17 Investigation of dyspepsia. bright red stool.

Management
Vomiting The principles of emergency management of non-variceal bleeding are
discussed in detail below. Management of variceal bleeding is discussed
Vomiting is a complex reex involving both autonomic and somatic neu- on page 882.
ral pathways. Synchronous contraction of the diaphragm, intercostal
muscles and abdominal muscles raises intra-abdominal pressure and, 1. Intravenous access
combined with relaxation of the lower oesophageal sphincter, results in The rst step is to gain intravenous access, ideally using two large-bore
forcible ejection of gastric contents. It is important to distinguish true cannulae.

23
Psychogenic
Central nervous system disorders
Alcoholism  Vestibular neuronitis
 Migraine
 Raised intracranial pressure
 Meningitis

Drugs
 NSAIDs
 Opiates
 Digoxin
 Antibiotics
 Cytotoxins

Gastroduodenal
 Peptic ulcer disease
Infections  Gastric cancer
 Hepatitis  Gastroparesis
 Gastroenteritis
 Urinary tract infection
Uraemia
The acute abdomen
 Appendicitis
Metabolic  Cholecystitis
 Diabetic ketoacidosis  Pancreatitis
 Addison’s disease  Intestinal obstruction

Fig. 23.18 Causes of vomiting. (NSAIDs = non-steroidal anti-inammatory drugs)

798  GASTROENTEROLOGY

23.16 Modied Blatchford score: risk stratication in acute 2. Initial clinical assessment
upper gastrointestinal bleeding  Dene circulatory status. Severe bleeding causes tachycardia, hypo-
Admission risk marker Score component value tension and oliguria. The patient is cold and sweating, and may be
agitated.
Blood urea
 Seek evidence of liver disease (p. 860). Jaundice, cutaneous stig-
≥ 25 mmol/L (70 mg/dL) 6 mata, hepatosplenomegaly and ascites may be present in decom-
10–25 mmol/L (28–70 mg/dL) 4 pensated cirrhosis.
8–10 mmol/L (22.4–28 mg/dL) 3  Identify comorbidity. The presence of cardiorespiratory, cerebro-
vascular or renal disease is important, both because these may be
6.5–8 mmol/L (18.2–22.4 mg/dL) 2
worsened by acute bleeding and because they increase the hazards
< 6.5 mmol/L (18.2 mg/dL) 0 of endoscopy and surgical operations. These comorbidities are,
Haemoglobin for men therefore, a common cause of death following acute gastrointestinal
haemorrhage, even after successful haemostasis.
< 100 g/L (10 g/dL) 6
100–119 g/L (10–11.9 g/dL) 3
3. Basic investigations
120–129 g/L (12–12.9 g/dL) 1
 Full blood count. Chronic or subacute bleeding leads to anaemia,
≥ 130 g/L (13 g/dL) 0 but the haemoglobin concentration may be normal after sudden,
Haemoglobin for women major bleeding until haemodilution occurs. Thrombocytopenia
< 100 g/L (10 g/dL) 6 may be a clue to the presence of hypersplenism in chronic liver
disease.
100–119 g/L (10–11.9 g/dL) 1
 Urea and electrolytes. This test may show evidence of renal failure.
≥ 120 g/L (12 g/dL) 0 The blood urea rises as the absorbed products of luminal blood are
Systolic blood pressure metabolised by the liver; an elevated blood urea with normal creati-
nine concentration implies severe bleeding.
< 90 mmHg 3
 Liver function tests. These may show evidence of chronic liver
90–99 mmHg 2 disease.
100–109 mmHg 1  Prothrombin time. Check when there is a clinical suggestion of liver
> 109 mmHg 0 disease or patients are anticoagulated.
 Cross-matching. At least 2 units of blood should be cross-matched
Other markers if a signicant bleed is suspected.
Presentation with syncope 2
4. Resuscitation
Hepatic disease 2
Intravenous crystalloid uids should be given to raise the blood pressure,
Cardiac failure 2
with a 500 ml bolus recommended over less than 15 minutes in haemo-
Pulse ≥ 100 beats/min 1 dynamically unstable patients. In most patients, blood should be trans-
Presentation with melaena 1 fused when haemoglobin is less than 70 g/L, although transfusion should
be considered at higher levels in those with haemodynamic instability or
None of the above 0
ischaemic heart disease.

Oesophagitis Liver Portal vein

(10%) disease thrombosis
Usually with
hiatus hernia Varices
(2 – 9%)
Helicobacter
NSAIDs pylori Retching

Peptic ulcer
(35 – 50%) Mallory–Weiss tear
(5%)

Vascular Cancer of
malformations stomach or
(5%) oesophagus
(2%)

Aortic graft
NSAIDs Alcohol

Aorto-duodenal
fistula Gastric erosions
(0.2%) (10 – 20%)

Fig. 23.19 Causes of acute upper gastrointestinal haemorrhage. Frequency is given in parentheses. (NSAIDs = non-steroidal anti-inammatory drugs)
 Presenting problems in gastrointestinal disease  799

5. Oxygen 8. Endoscopy
Oxygen saturations should be monitored with pulse oximetry, with a tar- This should be carried out after adequate resuscitation, ideally within
get saturation of 94%–98% and oxygen prescribed as required. 24 hours; it yields a diagnosis in approximately 80% of cases. Patients
with major endoscopic stigmata of recent haemorrhage (Fig. 23.20)
6. Antithrombotic drugs can be treated endoscopically using a thermal or mechanical modal-
An increasing number of individuals present with an upper gastrointesti- ity, such as a ‘heater probe’ or endoscopic clips, combined with injec-
nal bleed while using antithrombotic medication. Aspirin can be contin- tion of dilute adrenaline (epinephrine) into the bleeding point (‘dual
ued during an upper gastrointestinal bleed. P2Y12-receptor antagonists therapy’). A biologically inert haemostatic mineral powder (TC325,
(e.g. clopidogrel) should be temporarily stopped (unless prescribed fol- ‘haemospray’) can be used as rescue therapy when standard therapy
lowing coronary artery stenting), as well as warfarin and direct oral anti- fails. This may stop active bleeding and combined with PPI therapy
coagulant therapy. However, early reintroduction of these medications may prevent rebleeding, thus avoiding the need for surgery. Newer
should occur after haemostasis has been achieved to reduce thrombotic techniques, such as ‘over-the-scope clips’, may also be used as a
events and death. rescue therapy when standard therapy fails, treating large vessels or
brotic lesions. Patients found to have bled from varices should be
7. Proton pump inhibitor (PPI) therapy treated by band ligation (p. 883); balloon tamponade is another option
Intravenous PPI infusion should be given in non-variceal bleeding, in indi- if this fails, while arrangements are made for a transjugular intrahe-
viduals who have a high-risk ulcer post endoscopy (e.g. ulcers with a clot patic portosystemic shunt (TIPSS). Balloon tamponade can be asso-
and/or requiring endoscopic haemostasis). PPIs work by reducing gas- ciated with serious complications, and newer techniques, such as
tric acid secretion, neutralising intragastric pH, promoting clot stability by removable, self-expanding, covered metal oesophageal stents may
reducing pepsin-induced clot lysis and increasing platelet aggregation. be used as an alternative option.
While intravenous PPI infusion is most frequently used, intermittent intra-
venous PPI and oral high-dose PPI can be considered as alternatives. 9. Monitoring
Box 23.17 outlines some common PPIs used. Patients should be closely observed, with hourly measurements of pulse,
blood pressure, oxygen saturations and urine output.
23.17 Common proton pump inhibitors (PPIs) and dosage for 10. Radiology and surgery
peptic ulcer disease
Patients who have recurrent bleeding, where endoscopic attempts
Oral administration
at haemostasis have failed, should be considered for radiological or
Standard dose High dose surgical intervention. If available, angiographic control of bleeding
Lansoprazole 30 mg OD 30 mg BD is generally preferred to surgery in older, frail patients. If surgery is
required, the choice of operation depends on the site and diagnosis
Omeprazole 20 mg OD 40 mg OD
of the bleeding lesion. Duodenal ulcers are treated by under-running,
Pantoprazole 40 mg OD 40 mg BD with or without pyloroplasty. Under-running for gastric ulcers can also
Rabeprazole 20 mg OD 20 mg BD be carried out (a biopsy must be taken to exclude carcinoma). Local
Esomeprazole 20 mg OD 40 mg OD excision may be performed, but when neither is possible, partial gas-
trectomy is required.
Intravenous infusion
Dose 11. Eradication
Omeprazole 80 mg IV bolus, followed by 8 mg/hr for 72 hrs Following treatment for ulcer bleeding, all patients should avoid
Pantoprazole non-steroidal anti-inammatory drugs (NSAIDs) and those who test
Esomeprazole positive for H. pylori infection should receive eradication therapy
(BD = twice daily; IV = intravenous; OD = once daily)
(p. 814). Successful eradication should be conrmed by urea breath or 23
faecal antigen testing.

A B

Fig. 23.20 Major stigmata of recent haemorrhage and endoscopic treatment.

injection of adrenaline (epinephrine) and application of a heater probe.