Upper GI

Upper GI

Anatomy of the stomach

Physiology of the  stomach

Reservoir for digestion

Endocrine functions

• Secretion of gastrin(from antral  cells)
• Gastrin acts on parietal cells to  increase acid production

Exocrine functions- Acid secretion

PEPTIC ULCER DISEASE

Peptic ulcers are defects in the  gastric or duodenal mucosa  that extend through the  muscularis mucosa.

Occur when defensive  mechanisms ie. tight  intercellular junctions, mucus,  and epithelial renewal,  are  overcome by aggressive factors

PUD

Aggressive factors/Causitive factors

NSAIDS

H.Pylori

Severe physiologic stress- Burns, CNS trauma, Surgery

Hypersecretory states - Gastrinoma (Zollinger-Ellison syndrome), multiple endocrine neoplasia (MEN-I)

Patient Factors- 40-70 year, Men, Duodenal ulcers>gastric ulcers

Gastric ulcers	Duodenal ulcers
Same age group Males Located in prepyloric pyloric or coexist 70% located in lesser curvature Risk factor: Smoking, Alcolhol, Burns, Trauma, NSAIDS/steroids	Same age,sex Located mostly 2cm from  pylorus-duodenal bulb Caused by increase in gastric  acid
Epigastric pain Transiently relieved by food May be associated with nausea , vomiting  and decreased appetite	Burning or aching several hours  after a meal Haematemesis,FOB+ve Back pain Nausea, vomiting,decreased  appetite

Differential Diagnosis

Biliary Colic

Cholecystitis 

Cholelithiasis

Pancreatitis

Pancreatic Cancer

Acute Gastritis

Myocardial Infarction

Gastroesophageal Reflux Disease

Mesenteric Artery Ischemia

Diagnosing ulcers

Outpatient setting

Bloods

OGD

In the case of gastric ulcers biopsy should always be taken to outrule carcinoma . Patient  should be treated and rescoped  in approx 6 weeks to ensure  healing. Biopsies are taken on all  walls at 2 cm intervals

Medical treatment

Treat H pylori infection with  triple therapy

• PPI Clarithromycin penecillin
• PPI Metronidazole Ampicillin
• PPI Metronidazole Clarithromycin

Those not found to be H. Pylori  free- Treat with PPI or H2 receptor  blockers

Complications of PUD

Bleeding

Perforation

Pain

Obstruction- Secondary to repeated  inflammation and subsequent  scarring namely gastric outlet  obstruction

Indications for surgery

Similar in both types of  ulceration

• Refractory to treatment
• Haemorrhage
• Perforation
• Obstructive symptoms

Surgery is less common now  since the introduction of PPIs

Surgical management of  Gastric ulcers

Principles

• Remove ulcer
• remove gastrin secreting antrum

Billroth 1-remove distal third  of stomach and anastomose remainder to

duodenum

Billroth 2- remove distal 2/3rds of stomach and perform gastro-jejunostomy

Surgical management of  Duodenal ulcers

Principles- Reduce acid secretion by dividing the vagus nerve  (called a vagotomy)

Vagotomy denervates the stomach and therefore the pylorus which will lead to gastric outlet obstruction.

Therefore a drainage procedure is performed called a pyloroplasty.

2 surgical operations

• Truncal vagotomy and pyloroplasty
• Selective vagotomy and pyloroplasty

Vagotomy complications

• Decreased acid secretion (aim  of the game)
• Faster gastric emptying (loss of  vagally mediated)- Diarrhoea, Dumping syndrome
• Gastric outlet  obstruction(unless pyloroplasty  performed)
• Vagotomy complications
• Remember proximal vagotomy denervates from the stomach to the distal transverse colon including the pancreas and gallbladder
• Gallbladder denervation leads to stasis and which increases the chance of gallstones.
• Decrease in pancreatic and gallbladder secreations leading to undigested fats-steatorrhoea

Complications of  gastrectomy

Dumping syndrome

• Early v’s late
• Cardiovascular and GI symptoms  due to vagotomy and pyloroplasty  or gastrectomy
• Early DS due to hypovolaemia
• Late DS due to hypoglycaemia

Anaemia( Intrinsic factor essential for binding of Vit B12 for absorption in the terminal ileum)

Early satiety

Hypocalcaemia- reduced HCl prod interferes with absorption of calcium and Fe in the duodenum

Gastric Stump carcinoma? Due to chronic irritation of stump by acid duodenal secretions

Early Dumping  Syndrome	Late Dumping  Syndrome
No intact pylorus leads to dumping of large amounts of chyme,biliary and pancreatic secretions into duodenum at once Results in large fluid shift Occurs within 40 minutes of ingestion Symptoms include Tachycardia Diaphoresis Palpitations Diarrhoea Abdominal pain	Due to rebound hypoglycaemia Occurs 2-4 hours post op enterglucagon sensitizes islet cells overproduction of insulin Symptoms include Tachycardia Palpitations Diaphoresis Dizziness

Patient presenting with Haematemesis

• History and Examination
• Vital signs
• 2 large bore cannulae
• Bloods including FBC,U&E, Coag screen, Group and X match for 6 units, Inflammatory markers, Amylase
• If greater than 6 units required  urgent scope warranted.
• Oversewing of bleeding vessel.
• In the case of gastric ulceration  distal gastrectomy may be  warranted to excise the ulcer.
• No vagotomy required

Perforated Duodenal  Ulcer

Presentation

• Acute onset of epigastric pain
• Patients Vitals are ‘off’patient generally is unable to settle
• Nausea, vomiting
• O/E decreased bowel sounds, tenderness/rigidity of abdomen
• May complain of lower abdo pain as free fluid tracks down the paracolic gutters and causes local irritative symptoms.

Management of  Perforated DU

• 2 large bore cannulae
• Fluid resuscitation
• NG insertion
• Urinary catheter insertion
• Analgesia and antibiotics
• Bloods as before
• Erect CXR-Free air
• PFA- may see free air also
• CT abdomen- use water  soluble contrast. Given 1 hour  prior to scan to allow it to move  along the GIT tract.
• CT Abdomen findings include
  
  
  • Free air
  • Free fluid
  • Contrast may not fill small  intestine
  
  
  

Surgical Management

Graham patch

• Mini laparotomy from below umbilicus to epigastrium
• Stomach is identified and duodenum
• Perforation sought
• Omentum mobilised so that it is easily applied to site of perforation
• Suturedin 2 layers to peration site
• Closure

Definitions you should  know

• Cushings Ulcer- ulcer  associated with trauma, tumour  or neurology
• Curlings ulcer- associated with  major burns
• Marginal ulcer- ulceration at the  site of a GI anastomosis
• Dieulafoys ulcer-underlying  gastric malformation

GASTRIC CANCER

Adenocarcinoma

Risk factors

• Blood group A, male
• Pernicious anaemia (Autoimmune disease)
• Hypogammaglobulinaemia
• Previous partial gastrectomy
• Helicobacter pylori infection
• Atrophic gastritis
• Intestinal metaplasia

Presentation

Age group>60

Weight loss

Loss of appetite

Palpable epigastric mass

Melaena

Most present late and are not amenable to radical surgery

Investigations/Staging

CEA

OGD confirms diagnosis with a tissue biopsy

Endoscopic ultrasound may allow assessment of intramural tumour penetration

CT will assess nodal spread and extent of metastatic disease

Laparoscopy will identify peritoneal seeding

Survival

Overall 5 year survival is approximately 5%

Surgical options

No real role for adjuvant  therapy

Billroth 2 or Roux en Y  anastomosis

• Antrum-Distal subtotal(75%)  gastrectomy
• Body- total gastrectomy
• Proximal- total gastrectomy

Roux en Y anastomosis- Y-shaped anastomosis. After division of the small intestine,the distal end is implanted into the stomach and the proximal end into the small intestine below the anastomosis to provide drainage without reflux.

Virchow’s node- Metastatic gastric carcinoma in  the left supraclavicular fossa

Krukenburg tumour- Gastric ca which has  metastasized to the ovaries

Other Gastric tumour

Gastric Lymphoma

GIST tumour

The Stomach is the commonest extranodal primary site for non-Hodgkin's lymphoma Secondary Lymphoma is commonly seen in stomach from another site Accounts for 5% of gastric malignancies Presentation is similar to gastric carcinoma Anaemia and epigastric mass are common Age of presentation is approx 60 years Investigations EUS is the best modality Treatment 70% of tumours are resectable 5-year survival is approximately 25% Treatment modalities are discussed on a case by case basis at an MDT Treatments range from chemotherapy alone, H pylori eradication or surgery and chemotherapychemotherapy may be useful MALT lymphoma A type of primary gastric lymphoma The stomach does not usually contain  lymphoid tissue MALT follicles found in the stomach are  associated with H pylori infection Patients can be completely cured by H  pylori eradication or else use it in  conjunction with chemotherapy

Gastrointestinal stromal  tumours Previously classified as  Leiomyosarcomas,  Leiomyomas or sarcomatous  lesions ie they originate from  smooth muscle. There are classified according  to the degree of differentiation  towards different cells Classification Benign Differentiation toward muscle cells Differentiation toward neural  elements Malignant Dual differentiation Lacking differentiation 1% of stomach cancers Presentation Haemetemsis Melaena Epigastric mass Investigation EUS + biopsy Endoscopy Treatment Surgery-local excision of tumour Lymph node clearance  unnecessary as spread is not  common Large tumours may need formal  gastrectomy+/- adjuvant therapy Trials on a new drug Glivec  have  been shown to be effective

Sister Mary Joseph Nodule

• A 'nodule' in the umbilicus often associated with advanced malignancy
• Presents as firm, red, non-tender nodule
• Results from spread of tumour within the falciform ligament
• 90% of tumours are adenocarcinomas
• Commonest primaries are stomach and ovary
• Primary tumour is almost invariably inoperable

OESOPHAGUS

Oesophageal Anatomy

Superior 1/3rd-smooth muscle

Middle 1/3rd-mixed

Inferior 1/3rd-smooth muscle

Length -25cm

Oesophageal  constrictions

Superiorly: level of cricoid cartilage, juncture with pharynx-cricopharyngeal sphincter @15 cm

Middle: crossed by aorta and left main bronchus @22cm

Middle; L main Bronchus@27cm

Inferiorly: diaphragmatic sphincter @37cm

Why are constrictions  important

Areas where foreign bodies  lodge

Common sites of carcinoma

Difficulty passing scope on  OGD may occur

DYSPHAGIA

Definition-difficulty swallowing

Typical presentation in  oesophageal Ca is one of  progressive dysphagia starting  with solids followed by fluids

Odynophagia- pain on  swallowing

Differential diagnosis

Anatomical causes

Intrinsic to wall

• Carcinoma
• Cricoid web
• Inflammatory lesions

Extrinsic lesions

• Bronchial Ca
• Mitral stenosis leading to L atrial  enlargement

Functional lesions

Neurological causes

• Post CVA
• MND
• Globus hystericus-constriction of the lower part of the oeophagus associated with anxiety

Dysmotility- Achalasia, Diffuse oesophageal spasm, Scleroderma

Assessment

History and Examination

OGD+/-biopsy

Barium swallow

CT if suspect extrinsic  compression is the cause.

Other tests

• Oesophageal manometry
• pH studies- Naos oesophageal wire  containing a pH probe is left in  oesophagus for a 24 hour  period. If oesophageal pH is greater  than 4 for >4% of the time this  indicates reflux

Oesophageal  manometry

• NG tube passed into oesophagus
• Pressure transducer on tip of it measures resting and squeezing pressures at different levels of the oesophagus
• Normal peristaltic waves travel at a rate of 5cm/sec through oesophagus
• Normal resting pressure of LOS is 10-15mmHg
• Squeeze pressures should generate up to 100mmHg

pH studies

GORD

3 factors exist to keep gastric  juices out of the oesophagus

• LOS competence
• Oesophageal motility
• Clearance into stomach

Presentation

Pain- Epigastric, Retrosternal, Interscapular

Odynophagia

Reflux of food especially on bending

Pulmonary aspiration- Nocturnal coughing, Hoarse voice

Investigations             

• pH monitoring is the gold  standard investigation
• Rule out MI
• OGD + biopsy-5cm above GOJ  shows increased eosinophils and  hypoplasia
• See if patient has a hiatus hernia  (1/3 of patients with h.h have  GORD)

Complication of GORD

Oesophageal stricture

• Commonest cause
• Treat by balloon dilatation via  OGD
• Surgery options-Lap Nissan  fundoplication

Barrett’s oesophagus- Increased risk of malignant  transformation

Treatment of GORD

Conservative mgt-

Antacids, lose weight, raise head  of bed etc.

Metoclopramide,H2 blockers,  PPIs

Surgical

Nissan fundoplication- Fundus of stomach is  mobilised,wrapped around the  oesophagus

MOTILITY DISORDER

Primary

• Achalasia
• Diffuse oesophageal spasm

Secondary

• Autoimmune rheumatic disorders(scleroderma)
• Chagas disease(chronic infection with T cruzi associated with mega disorders)
• DM
• Amyloid

Achalasia	Diffuse oesophageal  spasm	Autoimmune diseases
HighLOS pressure leading to  failure of the sphincter to  relax poor peristalsis Presents with dysphagia and  retrosternal chest pain Affects 30-60 years age group Investigation;Barium swallowÞ   bird’s beak, lack of gastric air  bubble, contrast may not enter  stomach Treatment Balloon dilatation Heller’s cardiomyopathy-release  of muscle at the GOJ, reflux  common post op Injection of botulinum toxin at  ultrasound	Part of the differential of MI Symptoms- Retrosternal chest pain radiating  to jaw Invest;- Manometry-nutcracker  oesophagus Management- Nifedipine	Scleroderma- Srticture formation occurs due  to inflammation and GORD CREST syndrome- Calcinosis, Raynauds, Oesphagitis, Scleroderma, Telangiectasia Investigations- Manometry- incompetent LOS Treatment- Partial fundoplication Other; Rheumatoid Arthritis SLE Dermatomyositis Polymyositis May all be associated with  oesophageal dysmotility

OESOPHAGEAL CARCINOMA

Adenocarcinoma>SCC

Adeno seen in lower 1/3rd

SCCs can be any site

Males>Females

Age;>40

Most common at sites of physiological narrowing

Lower 1/3rd and GOJ most common sites

Oesophageal carcinoma

Risk factors

Adenocarcinoma	SCC
Barretts GORD Obesity Alcohol Cigarette smoking Oesophageal carcinoma Risk factors	Alcohol Smoking Coeliac Achalasia PUD

Symptoms

Dysphagia

Retrosternal pain

Coughing during eating

Pseudo-achalasia

Pre-operative

U&Es, FBC

Optimise nutrition-NG feed

Stop smoking etc

Surgical management

Ivor Lewis procedure

• Laparotomy and mobilisation of  stomach
• Right thoracotomy- resection of  tumour and reanastomosis of  stomach to healthy oesophagus

5 year survival 25% and only  30% patients suitable for  surgery!

Palliative treatment

• Intubation with metal stent under  radiological control
• Chemotherapy-adeno
• Radiotherapy-SCC

GASTRIC CANCER

Presentation

Indigestion

Nausea or vomiting,

Dysphagia

Postprandial fullness

Loss of appetite

Weight loss

Haematemasis, melena

Symptoms of metastatic disease

Palpable enlarged stomach

Succussion splash

Hepatomegaly

Periumbilical metastasis (Sister Mary Joseph nodule)

Virchow nodes                            

Blumer shelf (ie, shelflike tumor of the anterior rectal wall).

Anaemia

Jaundice

Aetiology

70’s

Higher incidence in Japan

Diet

Smoking

Helicobacter pylori infection

Previous gastric surgery

Genetic factors

• Hereditary nonpolyposis colorectal cancer
• Li-Fraumeni syndrome
• familial adenomatous polyposis
• Peutz-Jeghers syndrome. 

Pernicious anemia

Gastric ulcers

Obesity

Radiation exposure

Investigations

Labs

Ba Meal

CT abdomen

PET scan

Bone scan

OGD

Endoscopic ultrasound

Diagnostic laparoscopy

Histology

Adenocarcinoma 95%

Tubular

Papillary

Mucinous or signet-ring cells

Undifferentiated lesions.

Gastrointestinal stromal tumors 2%

Carcinoids (1%)

Adenoacanthomas (1%)

Squamous cell carcinomas (1%)

Gross appearence

Ulcerative

Polypoid

scirrhous (ie, diffuse linitis plastica)

superficial spreading

multicentric

Staging

TX - Primary tumor (T) cannot be assessed

T0 - No evidence of primary tumor

Tis - Carcinoma in situ, intraepithelial tumor without invasion of lamina propria

T1 - Tumor invades lamina propria or submucosa

T2 - Tumor invades muscularis propria or subserosa

T3 - Tumor penetrates serosa (ie, visceral peritoneum) without invasion of adjacent structures

T4 - Tumor invades adjacent structures

NX - Regional lymph nodes (N) cannot be assessed

N0 - No regional lymph node metastases

N1 - Metastasis in 1-6 regional lymph nodes

N2 - Metastasis in 7-15 regional lymph nodes

N3 - Metastasis in more than 15 regional lymph nodes

MX - Distant metastasis (M) cannot be assessed

M0 - No distant metastasis

M1 - Distant metastasis

Treatment

Medical

              Chemoradiotherapy, adjuvent v’s neoadjuvent

Surgical

              Gastroesophagectomy

              Total Gastrectomy

              Distal gastrectomy

              Lymph node disection

              D1 v’s D2 v’s D3, splenectomy

D1 includes perigastric lymph nodes,

D2 includes nodes along the hepatic, left gastric, celiac, and splenic arteries, and the splenic hilum,

D3 includes nodes within the porta hepatic and periaortic region.

Prognosis

              The 5-year survival rate for a curative surgical resection ranges

60-90% for patients with stage I

30-50% for patients with stage II disease

10-25% for patients with stage III disease