Approach to Chronic epigastric pain

1. Chronic Epigastric Pain L2
By: Dr. Jwan Ali Alsofi

2. Introduction
 Patients with chronic or recurrent epigastric pain
generally present electively to their general practitioner.
 They may subsequently be referred for specialist
consultation.
 Causes of chronic and of acute epigastric
pain thus differ somewhat in emphasis, but overlap.
 Chronic epigastric pain may be described by the patient
as:
 indigestion or dyspepsia (food-related discomfort) if
discomfort is less severe.
 fullness, bloating,
 pressure and hunger pain.
 Chronic pain associated with weight loss always
warrants thorough assessment and investigation.

3. ■ Parietal cells  PP(H+) & IF
■ Chief cells  pepsinogen
■ D cells  somatostatin
■ G cells  gastrin
■ enterochromaffin-like cells  Histamine ( in response to vagus nerve
and gastrin)
■ Parietal / chief cells  fundus / body
■ G/D cells  antrum
■ enterochromaffin-like cells  body
■ duodenal endocrine cells  secretin and cholecystokinin

4. Causes
I. Nonulcer dyspepsia(Functional disease)
2.Gallstones and chronic cholecystitis
3. PU
 DU
 GU
4. Chronic pancreatitis
5. Carcinoma of the stomach

5. CHRONIC EPIGASTRIC PAIN
History

6. Gallstones and chronic cholecystitis
• Patients with gallstones frequently present with episodic upper abdominal pain.
• Biliary pain (‘colic’) begins abruptly and subsides gradually over a period of hours
and is usually felt in the epigastrium or right hypochondrium.
• commonly radiates around the costal margin to the back or up to the right
shoulder, with a sometimes severe and constant nature.
• It can be postprandial or nocturnal
• There may be an association with fatty and/or oily food consumption.
• Patients have often had a number of similar attacks requiring analgesics or
assessment in an emergency department.
• The pain may occasionally be felt in the left hypochondrium or precordially,
making it difficult to distinguish from oesophageal pain or angina.
• The more severe and insistent acute upper abdominal pain of acute cholecystitis
usually leads to hospital admission and early cholecystectomy and is related to
persistent rather than transitory obstruction of the cystic duct by stone.
• Chronic or recurrent dyspeptic symptoms are also common. These may have been
present for many years and are associated with flatulence, abdominal distension,
nausea and fatty food intolerance.

7. Duodenal ulcer
• duodenal ulcer has a chronic, fluctuating, remitting and relapsing natural history.
• The pain is felt in the epigastrium , is described as dull, boring, aching, burning, gnawing or hunger-like.
• The pain is generally relieved by antacids, food and milk.
• A high intake of milk may produce weight gain, but occasionally food or alcohol can make the pain
worse, with associated weight loss.
• the patient localises the pain precisely in the epigastrium just to the right of the midline.
• posterior penetration of the ulcer with pancreatic irritation or inflammation:
1. Radiation directly to the back in the interscapular region.
2. loss of the cyclical character of the pain,
3. loss of response to antacids
4. vomiting.
• Periodicity and relapse of symptoms is classic :
1. Relapses and remissions follow each other in cycles.
2. Relapse is often triggered by smoking, stress or NSAIDs.
3. During relapse, attacks of pain come on each day, from ½ -3 hours after meals.
4. Relapses last for days or weeks and often occur during spring and autumn.
5. Remissions last for weeks to months.
6. In about half the patients, the daily cycle of pain during a relapse may occur so close to the next
meal that it is described as ‘hunger’ pain.
• Nocturnal pain is a common complaint, usually wakening the patient in the early morning hours and also
relieved by food and alkali.
• 90% of duodenal ulcers has been proven to be due to Helicobacter pylori..

8.  The Zollinger-Ellison syndrome (gastrinoma of the pancreas)
should be considered when a severe and resistant ulcer diathesis is
present. Features suggesting the diagnosis include:
1. multiple and recurrent ulcers,
2. ulcers situated more distally,
3. severe diarrhoea (found in 30% of cases)
4. the combination of severe upper and lower abdominal symptoms

9. Pathology of Doudenal Ulcer
• Most occur in the first part of the duodenum.
• A chronic ulcer penetrates the mucosa and into the muscle coat,
leading to fibrosis  The fibrosis causes deformities such as
pyloric stenosis.
• When an ulcer heals, a scar can be observed in the mucosa.
• Sometimes there may be more than one duodenal ulcer.
• The situation in which there is both a posterior and an anterior
duodenal ulcer is referred to as ‘kissing ulcers’.
• Anteriorly placed ulcers tend to perforate
• Posterior duodenal ulcers tend to bleed, sometimes by eroding
into the gastroduodenal artery.
• Occasionally, the ulceration may be so extensive that the entire
duodenal cap is ulcerated and devoid of mucosa.
• malignancy in duodenal ulcer is so uncommon that under normal
circumstances surgeons can be confident that they are dealing with
benign disease.  In the stomach the situation is different.

10. Histopathology of DU
1. Microscopically, destruction of muscular coat.
2. Base of ulcer covered with granulation tissue.
3. Arteries in region showing typical changes
(endarteritis obliterans).
4. Sometimes terminations of nerves can be seen
among fibrosis.

11. Gastric ulcer
• The history of patients with gastric ulcer is
very similar to that of duodenal ulcer.
• Pain, however, tends to be more severe,
more loss of work occurs
• relapse is more frequently triggered by anti-
inflammatory agents.
• Relapses last longer, generally 1–2
months.
• Food and alcohol appear to worsen the
pain,
• Pain generally occurs within 30 minutes of
a meal.
• Anorexia and weight loss are also more
common.
• Associated gastritis is a feature of gastric
ulcer and contributes to weight loss.
• Vomiting is more common and more likely
to relieve the pain.
• Ulcers on the lesser curvature are
associated with chronic gastritis, whilst
those on the greater curve are the result of
ingestion of NSAIDs

13. Investigations ofsuspected PU
 Gastroduodenoscopy(OGD)
 Investigation of choice in management of suspected
peptic ulceration.
 In hands of well-trained operator, highly accurate.
I. In stomach, any abnormal lesion multiple biopsied .
II. Biopsies of antrum taken (histological evidence of
gastritis).
III. A ‘U’ maneuver performed to exclude ulcers around
gastro-oesophageal junction.
 CLO test performed to determine the presence of H. pylori.

14. H.Pylori
• H.pylori live in low acid media of gastric mucosa (gastric antrum )and
through release of urease enzyme which produce strong alkali ammonia
which neutralize high acidity of stomach to protect itself
• Has ability to hydrolyse urea.
• Production of ammonia, a strong alkali.
• The ammonia = antral G cells = release of gastrin via the negative-
feedback loop.
• Hypergastrinaemia in patients with peptic ulcer disease.
• Result in gastric acid hyper secretion

16. Treatment of peptic ulceration
• Majority of uncomplicated peptic ulcers treated medically.
• Surgical treatment of uncomplicated peptic ulceration decreased since the
1960s.
• Surgery now seldom performed in the west.
• Surgical treatment was aimed principally at reducing gastric acid
secretion and, in the case of gastric ulceration, removing the
diseased mucosa.
• When originally devised, medical treatment also aimed to reduce
gastric acid secretion, initially using the highly successful H2-
receptor antagonist and, subsequently, proton pump inhibitors..
• Modifications to the patient’s lifestyle.
• PPI can effectively render a patient achlorhydric and all benign ulcers will
heal using these drugs, the majority within 2 weeks..
• Proton pump inhibitors safe and devoid of serious side-effects.
• The problem with all gastric antisecretory agents is that following cessation
of therapy relapse is almost universal.

17. Eradication therapy
 Eradication therapy now routinely given to PU.
 Complete eradication of organism cure the disease.
 Reinfection as an adult is uncommon.
 Eradication therapy mainstay treatment for PU.
 Extremely economical by comparison.
 Also safer than surgical treatment.
 H. pylori therapy:
 First Line:
– Amoxicillin and Clarithromycin –or-
– Clarithromycin and Flagyl (+)
– PPI (or H2 blocker).
 Treat for 7 – 14 days.
 Recheck for H. pylori after treatment.
 Continue acid suppression until ulcer is healed.

19. Surgical treatment of
uncomplicated peptic ulceration
 Peak in the 1960s.
 Incidence of surgery for uncomplicated peptic
ulceration fallen.
 Surgery now little more than historical interest.

20. Operations for duodenal ulceration
1. Billroth II gastrectomy
2. Gastrojejunostomy
3. Truncal vagotomy and drainage
4. Highly selective vagotomy
5. Truncal vagotomy and antrectomy

21. Billroth II
gastrectomy

22. Gastrojejunostomy
• Because of the potential for mortality after gastrectomy, the use of
gastrojejunostomy alone in the treatment of duodenal ulceration was developed.
• Reflux of alkali from the small bowel into the stomach reduced duodenal acid
exposure and was often successful in healing the ulcer.
• However, because the jejunal loop was exposed directly to gastric acid, stomal
ulceration was extremely common, hence the procedure in isolation was ineffective.

23. TrunkalVagotomy
• Section of the vagus nerves, which are critically involved in the secretion of gastric
acid, reduces the maximal acid output by approximately 50%.
• Because the vagal nerves are motor to the stomach, denervation of the
antropyloroduodenal segment results in gastric stasis in a substantial proportion of
patients on whom truncal vagotomy alone is performed. So what to do?!
• Drainage procedures have been performed also :
1. Pyloroplasty  performed to widen the pyloric sphincter
2. Gastrojejunostomy

24. Pyloroplasty

25. Highly SelectiveVagotomy
• The operation of highly
selective vagotomy in
which only the parietal
cell mass of the
stomach was
denervated.
• The most satisfactory
operation for duodenal
ulceration
• The operative mortality
was lower than any
other definitive
operation for duodenal
ulceration  bcz GIT
was not opened during
this procedure.
• The operation
disappeared from
routine use with the
advent of antisecretory
agents and eradication
therapy.

26. Truncal vagotomy and antrectomy
• In addition to a truncal vagotomy, the antrum of the stomach is removed, thus
removing the source of gastrin, and the gastric remnant is joined to the duodenum.

27. Operations for gastric ulcer
 Billroth I gastrectomy
• In contrast with duodenal ulcer surgery, when the principal objective was to reduce
duodenal acid exposure,
• in gastric ulceration the diseased tissue is usually removed as well.
• This has the advantage that malignancy can then be confidently excluded. As with duodenal
ulceration such surgery is not now performed except for complications of gastric ulcer.

28. Sequelae of peptic ulcer surgery
1. Recurrent ulceration
2. Small stomach syndrome
3. Bile vomiting
4. Early and late dumping
5. Post-vagotomy diarrhoea
6. Malignant transformation
7. Nutritional consequences
8. Gallstones

29. 5.Chronic pancreatitis:
• Progressively destroys exocrine and endocrine tissues of
pancreatic gland
 History:
• Middle aged ,80% occur in men
• Rare
• Severe recurrent upper abdominal pain
• Usually radiates to back
• Pain gnawing,dull,persistent ache
• Often related to episodes of excessive alcohol drinking
• May follow multiple attacks of acute pancreatitis
• Mostly due to chronic alcoholism
• Weight loss and nausea
• Diabetes , steatorrhoea, jaundice develop in 10%
• Drug addiction is common(narcotics)

30. CHRONIC EPIGASTRIC PAIN
Examination

31. Examination
 Few physical signs
 Patient look distraught
 Weight loss
 Jaundice
 Mass (pseudocyst) may be palpable in epigastrium
 Portal hypertension(portal vein thrombosis)

32. The complications of peptic ulceration
 The common complications of peptic ulcer are:
1. Perforation
• When perforation occurs anteriorly into the peritoneal cavity,
the patient presents with features of generalised peritonitis.
• Sometimes the perforation might occur posteriorly into the
lesser sac. In such a case, the peritonitis is contained with a
resultant perigastric abscess.
• Perforation requires resuscitation followed by operation –
biopsy and closure of the perforation.
2. Bleeding
3. Stenosis

35. Gastric Outlet Obstruction
 The common causes:
 Chronic duodenal
ulceration/fibrosis
 Antral gastric carcinoma
 Carcinoma of the head
of pancreas
 Rare causes:
 Variety of benign tumours
 Lymphoma
 Crohn,s disease
 Duodenal haematoma
 Adult pyloric hypertrophy
 Annular pancreas
 Mucosal diaphragm
 Willkie's disease(Arterio-
Mesenteric compression)

36. Gastric Outlet Obstruction(GOO)
• The two common causes are:
1. Gastric cancer
2. Pyloric stenosis due to PU.
• Previously, the latter was more common.
• Now, with the decrease in the incidence of peptic
ulceration and the advent of potent medical
treatments  gastric outlet obstruction should
be considered malignant until proven otherwise,
at least in resource-rich countries.

37. ■ The term ‘pyloric stenosis’ is normally a misnomer. The
stenosis is seldom at the pylorus.
■ Commonly, when the condition is due to underlying peptic
ulcer disease, the stenosis is found in the first part of the
duodenum, the most common site for a peptic ulcer.
■ True pyloric stenosis can occur due to fibrosis around a
pyloric channel ulcer.
■ Nowadays, as most patients with peptic ulcer symptoms are
treated medically, it is easy to understand why the condition
is becoming much less common.
■ In recent years the most common cause of gastric outlet
obstruction has been gastric cancer  In this circumstance
the metabolic consequences may be somewhat different
from those of benign pyloric stenosis because of the relative
hypochlorhydria found in patients with gastric cancer.

38. Clinical Features:
1. In benign gastric outlet obstruction there is usually a long history of peptic ulcer
disease.
2. Pain: In some patients the pain may become unremitting and in other cases it may
largely disappear.
3. Vomiting:
• The vomitus is characteristically unpleasant in nature and is totally lacking in bile.
• Very often it is possible to recognise foodstuff taken several days previously.
4. losing weight, and appears unwell and dehydrated.
• Fluid loss causes extreme dehydration seen clinically as sunken eyes, dry tongue
and loss of skin turgor.
• Tetany:
• carpo-pedal spasm because of tetany.
• Tetany is liable to occur in any form of alkalosis, in this case metabolic.
• This is because loss of H+ (normally bound to albumin) releases a place that is
taken up by free ionised Ca++, which is now bound to albumin thus reducing ionised
Ca++, resulting in tetany.
• O/E:
1. distended stomach
2. a succussion splash may be audible on shaking the patient’s abdomen.

40. Metabolic Effects:
• It is notable that the metabolic abnormalities may be less if the
obstruction is due to malignancy, as the acid–base disturbance is less
pronounced.
• The metabolic consequences of benign pyloric stenosis are unique:
• The vomiting of HCL results in hypochloraemic alkalosis.
• Initially the sodium and potassium may be relatively normal.
• As dehydration progresses, more profound metabolic abnormalities
arise, partly related to renal dysfunction.
• Initially, the urine has a low chloride and high bicarbonate content,
reflecting the primary metabolic abnormality.
• This HCO3 is excreted along with Na, and so with time the patient
becomes progressively hyponatraemic and more profoundly
dehydrated.
• Because of the dehydration, a phase of sodium retention follows and
potassium and hydrogen are excreted in preference. This results in
the urine becoming paradoxically acidic and hypokalaemia ensues.
Alkalosis leads to a lowering in the circulating ionised calcium, and
tetany can occur.

41. Management:
 Treating the patient involves:
I. correcting the metabolic abnormality
II. dealing with the mechanical problem.
1. Correcting dehydration: giving IV isotonic saline with
potassium supplementation.
2. Stomach should be emptied using NG tube and lavage.
3. The patient should also have a gastric antisecretory agent
(H2-receptor blocker or PPI), initially given IV to ensure
absorption.
• This then allows investigation of the patient:
1. Endoscopy done and biopsy taken to exclude malignancy.
2. Contrast radiology also used to diagnose.
 Early cases resolve on conservative treatment (as the oedema around
the ulcer diminishes as the ulcer is healed).
 Endoscopic treatment with balloon dilatation has been practised and
may be most useful in early cases.
 Severe cases are treated surgically  Gastro-Enterostomy+ Vagotomy.

42. Other causes of GOO:
Adult pyloric stenosis
• a rare condition
• its relationship to the childhood condition is unclear,
• some patients have a long history of problems with gastric
emptying.
• It is commonly treated by pyloroplasty rather than
pyloromyotomy.
Pyloric mucosal diaphragm
• Origin of this rare condition unknown.
• Usually not become apparent until middle life.
• When found: simple excision of mucosal diaphragm is all
that is required..

43. ■ A barium meal would show
smooth cut-off at
pyloroduodenal junction where
there is total obstruction with
massive gastric dilatation with a
large amount of food residue.

45. 5. Carcinoma of the stomach
• Carcinoma of stomach major cause of cancer mortality
worldwide.
• Prognosis tends to be poor.
• Cure rates little better than 5–10%.
• Better results are obtained in Japan(disease common).
• Gastric cancer curable disease (provided detected at
appropriate stage).
• The only treatment modality able to cure the disease is
resectional surgery.
• Stomach cancer should be suspected when dyspepsia
starts for first time over 40 years
• Early gastric cancer, with minimal mucosal changes,
needs to be diagnosed if prognosis is to be improved.
• Unfortunately many patients present (or are diagnosed)
late in Western countries.

46. Incidence
 In UK incidence =15 cases/100 000 population /year.
 In USA 10 cases/100 000 population /year.
 In Eastern Europe 40 cases /100 000 population/year.
 In Japan disease much more common, incidence =70 cases /100000
population /year.
 Men more affected than women.
 Incidence increases with age.
 Incidence of gastric cancer continuing to fall.
Carcinoma in proximal
stomach, oesophagogastric
junction
Carcinoma of distal stomach
and body
Incidence are rising Incidence are lowering
most common in higher
socio-economic groups
most common in low
socio-economic groups
not associated with H
.
.Pylori associated with H.Pylori

47. Aetiology
 Gastric cancer is a multifactorial disease:
1. Epidemiological studies point to a role for H. pylori
• Insufficient evidence to support eradication programs?
2. Gastric polyps (adenomatous).
3. Peptic ulcer surgery,four times the average risk.
4. Intestinal metaplasia.
5. Cigarette smoking.
6. Dust ingestion.
7. Diet (spirits, excessive salt intake, antioxidant deficiency, N-
nitroso compounds ).
8. Aetiology of proximal gastric cancer (not with Helicobacter
, obesity and higher socio-economic status).
9. Genetic factors

48. Pathology
 Lauren classification:
1. Intestinal gastric cancer(arises in areas of intestinal
metaplasia).
2. Diffuse gastric cancer( infiltrates deeply into the
stomach wall,linitis plastica,worse prognosis).
3. Mixed types(small proportion of gastric cancers).
 Other classifications
1. Early gastric cancer:
o cancer limited to mucosa and submucosa with or
without LN involvement (T1 any N).
o protruding, superficial or excavated.
o Early gastric cancer curable.
o 5-year survival rates in the region of 90%.
2. Advanced gastric cancer=involves muscularis.

49. Linitis Plastica

50. Clinical features of gastric Ca. :
 Traditionally gastric cancer has been described as presenting with
the three A’s – anaemia, asthenia and anorexia.
 Symptoms usually begin with lethargy and vague postprandial
heaviness, discomfort and fullness: a symptom complex usually
described as indigestion or dyspepsia.
 Anorexia is an early symptom
 weight loss, early satiety is a common feature, with
distortion of the senses of smell and taste
 Most patients have lost more than 5% of their normal body weigh
on presentation
 Continuous intractable epigastric pain is present.
 Nausea and vomiting can result from pyloric obstruction
 Dysphagia due to oesophageal obstruction(10% of patients)
 Haematemesis and maelena is unusual
 IDA is found in nearly half of cases (from chronic blood loss)

51. Clinical Features:
 Advanced gastric cancer usually obvious
 Curable gastric cancer has no specific features (benign
dyspepsia?)
 key to improving outcome of gastric cancer (early
diagnosis)
 In west, early diagnosis more difficult (population
incidence much lower)
 Gastric anti-secretory agents improve symptoms of
gastric cancer
 Disease should be excluded before therapy started

52. Clinical Features cont,d

Advanced cancer, early satiety, bloating, distension,
vomiting.

Tumour frequently bleeds, resulting iron-deficiency
anaemia.

Obstruction leads to dysphagia, epigastric fullness o
r
vomiting.
 Pyloric involvement =Gastric Outlet Obstruction.

Left supraclavicular fossa (Virchow’s node, Troisier’s sign).

GOO more commonly associated with malignancy?

Non-metastatic effects of malignancy (thrombophlebitis
=Trousseau’s sign) ,DVT.

Result from effects of tumour on thrombotic and
haemostatic mechanisms.

53.  Rarely disseminates before involved lymph nodes.
 Opportunity to cure prior to dissemination.
 Early diagnosis key to success.
 Late presentation is cause of poor survival figures.
 Only treatment modality cure the disease
resectional surgery.

54. Staging: T N M classification
• T1 Tumor involves lamina propria or submucosa.
• T2Tumor invades muscularis
• T3Tumor involves serosa
• T4Tumor invades adjacent organs
 N0no LN node metastasis
 N1metastasis to perigastric nodes
 N2 metastasis to LN along main arterial trunks
 M0no distant metastasis
 M1 distant metastasis ( which include peritoneum and N3/N4 nodes).
Ia T1 N0 M0 IIIa T2 N2 M0
Ib T1 N1 M0 T3 N1 M0
T4 N0 M0
II T1 N2 M0 IIIb T3 N2 M0
T2 N1 M0 T4 N2 M0
T3 N0 M0 IV T4 N2 M0

55. Spread of the carcinoma:
• Uncommonly involves distant metastasis before local spread)
• Diffuse type spreads via submucosal and subserosal lymphatic plexus
Direct spread:
• Tumor penetrates muscularis,serosa and adjacent
organs (pancreas,colon and liver)
Lymphatic spread:
• Spread to regional LNs and along main arteries, supraclavicular
LNs ( Trosier’s sign ).
• Nodal involvement does not imply systemic spread.
Blood borne metastasis:
• To the liver, lung and bone.
Trans peritoneal spread:
 If tumor reaches the serosa, it means incurability.
 It commonly causes ascites.
 Advanced peritoneal disease may be palpated abdominally or
rectally (tumor Shelf).
 Ovaries may be involved (krukenberg tumors).
 May spread to the umbilicus ( sister Joseph’s nodule)

56. Operation:
Incurable disease means either :
1. Fixation to the structures.
 It is important to note that involvement of
another organ per se does not imply
incurability, provided that it can be removed.
2. Hematogenous spread.
3. Involvement of distant peritoneum.
4. N4 nodal involvement.

57. Operation types:
 Total gastrectomy
• Upper mid line incision ,removal of entire greater and
lesser omentum .
• Removal of LNs along arteries supplying the stomach.
 Radical gastrectomy
• Removes spleen and distal pancreas and LN along
splenic artery.
 Subtotal gastrectomy
•Used for tumors distally placed , proximal stomach is
preserved .
 Palliative surgery
•Advanced disease or suffering from bleeding or
obstruction.
•Palliative resection of tumor with reconstruction of GIT
•Prognosis is poor.
•For tumors in cardia palliative tube could be used.

58. Total Gastrectomy

59. Summary
 Chronic epigastric pain usually present as indigestion
 Most causes of CEP are similar to acute epigastric pain but in less
severe forms
 History and examinations can help to reach diagnosis in most cases.
 Most common causes of CEP due to peptic ulcer disease.
 Main complications of PU: perforation, bleeding and pyloric
obstruction.
 Most of complications need invasive and semi invasive
procedure.
 Incidence of GC falling in some countries worldwide.
 In japan incidence high and they have best result for treatment.
 Early gastric cancer can be cured.
 Only modality of treatment is surgery.
 Lymph node clearance is important step in management of GC.