6.

UPPER GIT

1. APPROACH TO BLEEDING UPPER GIT

CAUSES

Variceal vs Non-variceal!

1. Peptic ulcer disease (bleeding peptic ulcer)

2. Gastritis, gastric erosions, duodenitis
3. Gastric malignancy
4. Stress ulcers from burns/ instrumentation
5. Gastro-oesophageal varices
6. Mallory-Weiss tear
7. Rare causes: AV malformation (Dieulafoy lesion) most will stop bleeding spontaneously, aortoenteric fistula
8. Bleeding from other sources: Haemoptysis, nasopharyngeal bleeding
9. Systemic: coagulopathies, renal failure (uraemic gastritis)

HISTORY (if patient is stable)

1. Nature of bleeding

Haematemesis
- [oes] Can be fresh red blood as in variceal bleeding, Mallory-Weiss tear, AV malformation
- [gastric] Coffee grounds vomitus is altered blood (due to gastric acid) and can come from gastric ulcer, gastritis/erosions, or variceal
blood that has entered the stomach [oes]

Malaena
- Altered blood; malaena indicates bleeding from the upper GIT i.e. above the ligament of Treitz
- Different types of malaena:
(a) Fresh malaena jet black with sheen, tarry, non-particulate (almost liquid in consistency), foul smelling, floats on water
maroon when you spread it out on gloves
(b) Stale malaena black-grey, dull, mixed with normal stool, occasionally particulate
(c) Iron stool greenish hue on rubbing between gloved fingers, particulate.
- If gloved finger is stirred in a cup of water, malaena will dissolve completely with no sedimentation and turn the water black, but iron
stool will sedimentate and turn the water green

Frank PR bleeding
- Very brisk upper GI bleed can present as frank PR bleeding as blood passes down so fast it doesnt get altered

2. Amount of blood

- If patient is having haematemesis, ask how much blood Cup? Bowl?

- Hematemesis: easily 1.5L of blood in stomach before vomiting out (bleeding more than pylorus can empty)

3. Aetiological clues / RF

Gastric ulcer/gastritis/erosions
- Any history of dyspepsia, gastric ulcer (any OGD done in the past showing these problems? On any gastric medications?)
- Any drugs that may predispose NSAIDs, antiplatelets, steroids, anticoagulants, TCM
Varices
- Any history of chronic liver disease
- Previous variceal bleeds
Mallory-Weiss tear
- Binge-drinking with subsequent severe retching and vomiting leading to haemetemesis
Malignancy
- Recent constitutional symptoms e.g. LOA, LOW, malaise
- Early satiety
- Dyspepsia

4. Complications

- Symptoms of anaemia: postural giddiness, shortness of breath, lethargy, effort tolerance, palpitations, chest pain
- AMI esp. if its an old patient with previous history of IHD

5. Comorbidities

- Elderly patient (>60) high risk (Rockall score)

- Other comorbidities: liver disease, renal disease, IHD high risk (Rockall score)
PHYSICAL EXAMINATION

1. Vitals!
- Blood pressure, heart rate stable? Any postural hypotension? (Tachycardia is an early sign of shock)
Narrowing pulse pressure (ind systolic hypotension) - check if patient is on BB!!
- RR>20
- Patients conscious level confused? (shock)
- Compare current vitals with vitals in ambulance, ED is there a worsening trend?
- Urine output: renal perfusion indicates cardiac output

2. General inspection
- Pallor
- Cold clammy peripheries impending shock
- Stigmata of chronic liver disease

3. Peripheries
- Cold clammy peripheries impending shock
- LN (mets)

4. Abdomen
- Any tenderness (not very helpful), epig mass
- Distension (++ blood in stomach)

5. Digital rectal examination

- Malaena or frank blood
- tumor deposits / rectal mass

IMMEDIATE MANAGEMENT

1. Resuscitation

- ABC: Protect airway, supplemental oxygen, 2 large-bore IV cannula in antecubital fossa

Bloods:
1. FBC (Hb will not drop in first 24hrs, low plt - may not stop bleeding),
2. U/E/Cr (dehydration - raised Ur more than Cr, elec abn from vomiting)
3. PT/PTT (check and correct for coagulopathy),
4. LFT (Child's score - ind etiology and outcome) - do in alcoholic hx or liver disease
5. GXM: order in active bleed 4 pints PCT, FFP, Plt
ECG to detect any acute myocardial ischaemia/infarction, PFO
CXR: PFO, aspiration, perforation if pt complains of pain
- Infusion
- 1 pint N/S over half to one hour if patient is in shock, followed by more fluids if necessary (be wary in pts with renal & heart failure)
- Packed cells if Hb is less than 10, to keep Hb above 10g/dL
- May consider platelets if patient is on antiplatelet meds (qualitative defect in platelets - even if plt is normal, they are dysfunctional)
- FFP if patient is on anticoagulants or PT/PTT prolonged (+ vitamin K)

2. Adjuncts

- NG tube if patient is having haematemesis prevents aspiration, allows gastric lavage prior to OGD (DO NOT insert if suspect varices)
- Catheterisation monitor I/O balance esp in elderly or when large amount of fluid resuscitation required, or anticipating surgery
- Intubate if: 1) massive uncontrolled active hematemesis
2) signs of decompensation eg. obtunded

3. Early medications

- IV omeprazole 80mg bolus --> 8mg/hr infusion X 3/7

stomach pH and stabilises clot formation
regimen to prevent rebleed (normal Tx dose 40mg bd)
- If suspecting varices IV somatostatin/octreotide, IV antibiotics
- Stop antiplatelets, anticoagulants, NSAIDS

4. Close monitoring

- Monitor for: SHOCK ( HR, BP, urine output, confusion & lethargy)
- HD with hourly para if
Elderly with many comorbidities
Hypotension

5. Emergency oesophagogastroduodenoscopy
 Alternatively, scope the next available OGD (usually following day)

- 3 Indications:
1. Shock / hemodynamic instability (ensure BP is stable before OGD - requires sedation)
2. Active BGIT (esp hematemesis, also fresh malaena)
3. Suspected variceal bleed
Not just low Hb as emergency scope causes more stress.
- Ensure bloods are running before OGD!
- Role of endoscopy
Diagnostic:
confirm UBGIT & identify source of bleeding,
Biopsy (+ CLO test if ulcer)
Therapeutic:
1. Varices: ligation/sclerotherapy, glue
2. Non-variceal: Clip, Coag, Injection
- CI: Perforation - air sufflation during OGD will cause
abdominal compartment syndrome --> decrease venous return --> patient may DIE
splinting of the diaphragm

- Repeat OGD with greater detail if it is normal the 1 st time.

Exclude haemoptysis & bleeding from nasopharynx
Look for Mallory weiss tear and posterior wall D1 bleeding ulcer (gastroduodenal artery)

Obscure overt bleed:

OGD normal Colonoscopy normal Small bowel imaging:
a) Capsule endoscopy
b) Tagged RBC
c) CT enterography
CT mesenteric angio anytime when patient becomes unstable.
2. VARICEAL BLEEDING

PATHOPHYSIOLOGY WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT

A result of portal hypertension (i.e. portal venous pressure >20 cmH2O - Previous history of variceal bleed
or >12 mmHg normal = 7-14 cmH2O / 5-10 mmHg) - Chronic alcohol intake
- Jaundice or stigmata of chronic liver disease
- Profuse hematemesis
MANAGEMENT OF VARICES can be divided into three categories:
1. Acute bleeding
2. Prophylaxis
3. Chronic management

I. ACUTE BLEEDING MANAGEMENT

1. Resuscitate
- Airway, breathing, circulation
- If patient appears well, look for early signs of shock tachycardia, postural hypotension
- Look at hydration status

2. Assess mental state

- If patient has altered mental state (encephalopathy) need to protect airway (may require intubation)

3. Vascular access, fluids/blood resuscitation, and blood investigations

- 2 large-bore IV cannula in proximal veins (cubital, EJV, IJV)
- Send bloods GXM 4 pints, FBC, U/E/Cr, LFT, PT/PTT
- Infuse fluids
- Under-resuscitate in variceal bleed (cf ulcer bleed) to keep Hb around 9, enthusiastic transfusion can portal pressure

4. Management of severe bleeding: Sengstaken-Blakemore tube

- If hypotensive and bleeding is ongoing, may require use of Sengstaken-Blakemore tube for up to 48hr (if unable to ligate)
- Protect airway before inserting tube.
- Inflate gastric balloon and pull upwards against cardioesophageal junction (balloon will press on perforator veins entering oesophagus
from stomach, and thus decrease oesophageal variceal bleeding); oesophageal balloon is not inflated nowadays

5. IV somatostatin or S/C Octreotide (Not given in ulcer bleed)

- Mode of action: splanchnic vasoconstrictor which portal blood flow and hence portal pressures variceal bleeding
- Also acts indirectly to inhibit secretion of gut hormones that increase portal blood flow

6. Acid suppression
- Increasing intragastric pH increases clot stability, aids haemostasis
- Agents available: omeprazole (Losec), esomeprazole (Nexium), pantoprazole, etc.

7. Antibiotics
- Not given in ulcer bleed
- Risk of sepsis in patients with CLD and bleeding
- Studies have shown that cover with broad spectrum Abx (Gram neg cover) infectious cx, mortality, and also risk of recurrent bleed
- Ceftriaxone, Ciproflox 1g/day
- Preferably started before endoscopy (procedures increase bacteraemia)

8. Emergency endoscopy
- Purpose: confirm diagnosis and institute management
- Needs to be done emergently (on admission) as soon as patient is stabilised since bleeding can be torrential and life-threatening
- Intervene if ESRF present or active bleed (not electively)
- Banding/Ligation is the best modality for oesophageal variceal bleeding (sclerotherapy a/w higher morbidity e.g. mucosal ulceration)
- Gastric varices are usually too large to be banded, sclerotherapy/ Glue (Histoacryl) used instead risk of embolism from histoacryl

9. Observation
- Keep patient in ICU!
- NBM 2-3/7
- Continue antibiotics and omeprazole
- Continue somatostatin up to the point where haemostasis is achieved or 5 days (exact ideal duration not well studied)
- Antiencephalopathy Tx: Lactulose + Cipro (clear gut to prevent absorption of NH3)
- Anticipate complications:
(a) encephalopathy fleet and lactulose, treat hypokalaemia from vomiting
(b) aspiration protect airway; ?benefit of gastric decompression using NG tube
(c) risks of procedure OGD-related risks

10. Management of possible precipitants

- NSAIDs; Hepatic vein thrombosis
If bleeding stops, home in around 1/52 Rescope before home! (ligate if rebleed)
If bleeding is not remediable by endoscopic intervention:

A. Insert Sengstaken-Blakemore tube up to 48hr (only temporary) repeat endoscopy 10-12 hours later
If rebleed after 48hr of SBT: consider surgery

B. TIPSS: Radiologically guided insertion of transjugular intrahepatic porto-systemic shunt

- If patient in good Childs score, to avoid as it ppt. encephalopathy
- Constant monitoring of patient.
- Cx: encephalopathy (increased risk with bigger shunt), bleeding, thrombosis, failure (blood flow in opposite direction)
- usually temporising procedure

C. Shunt surgery
Portocaval shunts (portal vein to IVC)
side-to-side, end-to-side
Mesocaval shunts (sup mesenteric vein to IVC)
Proximal splenorenal shunt (splenectomy with end-to-
side anastomosis of portal side of splenic vein to left
renal vein)
Distal splenorenal shunt (Warren-Zeppa shunt
splenic vein divided, splenic side anastomosed end-to- A. Normal liver with normal blood flow. B. End to side spelnorenal shunt.
side to left renal vein) C. End to side portacaval shunt. D. Mesocaval H-graft shunt

D. Sugiura procedure: last resort

Most effective non-shunt operation
A key point is that the left gastric (coronary) vein and the paraesophageal collateral veins are preserved to permit portoazygous
collateralization, which inhibits future varix formation
Japan cited a 5.2% operative mortality and a 6.3% rate of recurrent hemorrhage. In United States, operative mortality with this
procedure has exceeded 20%, with bleeding recurring in 35% to 55% of patients.

Splenectomy
Proximal gastric devascularisation
Selective vagotomy
Pyloroplasty
Oesophageal devascularisation
Oesophageal transection
II. PROPHYLAXIS OF VARICEAL BLEEDING

SECONDARY = Band ligation + Non-selective beta-blockers

- Best option is combination
propranolol unless CI: decrease size and prevent rebleeding
3 weekly ligation until completely obliterated

PRIMARY = Non-selective beta-blockers

(oesophageal varices with no previous history of variceal hemorrhage)

In pts with small varices with no risk of bleeding, the use of propranolol is of questionable benefit repeat OGD to monitor varices.
- cardiac output by 1 blockade and splanchnic blood flow by blocking vasodilating 2 receptors at splanchnic vasculature
- The use of beta-blockers decreases the risk of initial variceal bleeding by approximately 45%, to be continued indefinitely
- The dose: determined by a 20% decrease in baseline resting HR / decrease in HR to 55 bpm / dev adverse effects
- If contraindications to using beta-blockers exist, long-acting nitrates (eg, isosorbide 5-mononitrate) are alternatives
- Band ligation/ Sclerotherapy: not used as primary prevention. as effective as treatment with propranolol

Predictors of variceal haemorrhage: [SRCPS]

1 Site: varices at the GE junction have the thinnest coat of supporting tissue and are at highest risk of rupture and bleeding

2 Size:
F1: Small straight varices
F2: Enlarged tortuous varices that occupy less than one-third of the lumen
F3: Large coil-shaped varices that occupy more than one-third of the lumen

3 Childs score patients with higher Childs score have higher risk

4 Red signs:
Red wale marks (longitudinal red streaks)
(ESRH) Cherry red spots (flat discrete spots)
Haematocystic spots (raised discrete spots resemble blood blisters)
Diffuse erythema

5 Previous variceal haemorrhage:

70% of patients will have further variceal bleeds after an index bleed (risk highest in first 48 hours after first bleed)
30% rebleed within 6 weeks; 30% rebleed after 6 weeks

III. CHRONIC MANAGEMENT

- Start patient on an ablation regimen (endoscopy with initial ligation/sclerotherapy and subsequent endoscopic monitoring and
repeated ligation/sclerotherapy as required to completely ablate varices)
- If patient bleeds again failed ablation consider surgery (as above shunts, or Sugiura)
- LT propanolol + PPI
- Refer to Hepato for liver disease

http://www.heart-intl.net/HEART/011507/PortalHypertension.htm
3. PEPTIC ULCER DISEASE

EPIDEMIOLOGY
- Incidence about 100 per 100,000 per year
- 68% of patients are over 60 years of age
- Overall mortality 7-10%, unchanged for last 20yrs mostly due to ulcer bleeding esp in elderly with significant comorbidities

MAIN AETIOLOGICAL FACTORS

H. pylori
- 60% of population are positive for H. pylori by age 21
- About 10-20% of infected patients develop an ulcer
- Accounts for 90-95% of duodenal ulcers, and 50% of gastric ulcers

NSAIDs
- Accounts for most of the rest of ulcer disease not caused by H. pylori
- 30% of patients on NSAIDs will get an ulcer, of which 20% (6% overall) will have a clinically significant ulcer i.e. symptomatic, bleeding

Other factors
- Cigarette smoking
- Alcohol
- Steroids and anticoagulants do not increase the risk of ulcer formation, but increase the risk of bleeding in an existent ulcer

PATHOGENESIS

- An imbalance between mucosal protective mechanisms against acid, and aggressive forces that damage the gastric mucosa
- 2 Aggressive forces: gastric activity and pepsin activity
- 5 Protective mechanisms: mucus secretion, bicarbonate secretion into mucus, robust mucosal blood flow to remove protons, epithelial
regenerative capacity, prostaglandin secretion by mucosa to maintain blood flow
- H. pylori causes a local inflammatory reaction and secretes enzymes that break down the gastric mucosal barrier, and also enhances gastric
acid secretion and decreases bicarbonate production
- NSAIDs impair mucosal prostaglandin production (through non-selective COX inhibition) prostaglandins are important for mucosal
bicarbonate and mucin production and inhibiting gastric acid secretion, as well as maintaining mucosal blood flow

PRESENTATION

1. Incidentally detected on OGD

2. Symptoms of dyspepsia
(a) Ulcer-like dyspepsia: pain in the upper abdomen is the predominant symptom
(b) Dysmotility-like dyspepsia: non-painful discomfort in upper abdo, a/w upper abdo fullness, early satiety, bloating, belching, nausea
(c) Unspecified dyspepsia
- Pain is usually worse with food in a gastric ulcer, while it is relieved by food in a duodenal ulcer

3. Bleed
- As above, presenting with haematemesis (coffee-grounds vomitus) or malaena

4. Perforation
- Patient presents with sudden generalised abdominal pain that is aggravated by even the slightest movements
- Board-like rigidity, guarding will be present on examination (signs of peritonism)
- Erect CXR will show air under diaphragm

ENDOSCOPY (OGD)

- The most important and valuable investigation

- Roles of endoscopy:

(a) Diagnosis
Confirmation of ulcer disease
Location of ulcer
Biopsy to rule out malignancy esp gastric (usually 6 bites)
Biopsy of antral tissue for CLO (Campylobacter-like organism) test / rapid urease test for H. pylori: biopsy tissue is placed into a
medium containing urea and an indicator such as phenol red. The urease produced by H. pylori hydrolyzes urea to ammonia, which
raises the pH of the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE).
 (b) Prognostication of bleeding risk (in UBGIT)
Forrest classification (or endoscopic stigmata of recent haemorrhage ESRH)

Forrest grade Bleeding risk

1a Spurting (arterial) 90%
1b Non-spurting, ooze (venous) 20%
2a Non-bleeding ulcer with visible vessel 40%
2b Non-bleeding ulcer with adherent clot 20%
2c Ulcer with haematin-covered base (flat spot) 10%
3 Ulcer with clean base 5%
Adherent clot must flush and remove clot --> grade ulcer again

Classical bleeding BV: posterior-D1 (gastroduodenal art)

Tx: Only pigmented spot can leave alone, the rest must intervene!

(c) Endotherapy (in UBGIT)

1. Injection with adrenaline (1:10,000 dilute to 10ml - continue with N/S if need more) or absolute alcohol tamponade effect is the most
effective. Also vasoconstriction for adrenaline.
Inject around ulcer (4 quadrants). Cx: perforation, bleeding, necrosis, arrhythmia.
2. Coagulation (Heater probe = thermal / Argon plasma)
3. Haemostatic clipping (endoclip)

Principle: Dual modality better than single (as less risk of recurrent bleed and mortality) --> Usually Injection + Clip/Heater probe
No study proves superiority of either therapy.

Failed OGD hemostasis (after 1hr)

a) Surgery is mainstay
b) Transcatheter embolisation
a. ind: failed surgery, rebleed post-Sx (usually GDA), not fit for Sx
b. identify bleeding vessel and embolise with
i. Mechanical (non-absorbable coil eg. Titanium)
ii. Chemical (gel foam): can recannulise again in 2/52
c. Sandwich technique: embolise both prox and distal ends of vessel as bleeding can occur both ways.

Post-endotherapy:
- Monitor for rebleed = drop in Hb (not malaena / vomit blood clots as these are expected. Changes in vitals may be too late.)
- Diet individualised: usually NBM 1-2/7, 3/7 if worrisome, <1/7 if straight forward ulcer
- Re-scope the following day if youre worried about the outcome from the first scope (notroutine)
- Oralise PPI after 3/7 infusion (if worrisome, can give IV bolus PPI BD)
- TCU 3-4/52 at clinic

Re-scope in 6 weeks to document ulcer healing

If ulcer still present, biopsy ulcer again
1. Histo: exclude malignancy for gastric ulcer
2. Gastric biopsy urease test (to confirm eradication of H. pylori) - not accurate if patient on triple tx
Rescope and biopsy every 6/52 until ulcer is healed resect if persistent
Confirm eradication of H Pylori: Urease breath test, Re-biopsy
CONSERVATIVE MANAGEMENT

1. Gastroprotection

(a) Standard dose proton pump inhibitor

20mg OM
Promotes ulcer healing even with ongoing NSAID use
(b) Double dose famotidine
40mg BD
Inferior to omeprazole as famotidine only promotes ulcer healing if NSAIDs are stopped; ulcers will not heal with ongoing
NSAID therapy

2. H. pylori eradication

First line triple therapy: omeprazole 40mg BD (for 6 weeks), amoxicillin 1g BD, clarithromycin 500mg BD for 7 days
In penicillin-allergic patients, substitute amoxicillin with metronidazole 400mg BD
Document eradication by endoscopy with CLO test, urea breath test or stool serology testing
Treatment failure occurs in up to 20%
- treat with quadruple therapy: colloidal bismuth subcitrate 120mg QDS, tetracycline 500mg QDS, metronidazole 400mg
BD, omeprazole 20mg BD for 7 days

SURGICAL MANAGEMENT

Indications for surgery for acute PUD:

1. Bleed: Mainstay of Tx for failed OGD hemostasis (after 1hr)
2. Perforation

Indications for surgery for chronic PUD:

1. Recurrent bleeding
2. Splitting BV difficult to clip
3. Prev episode of shock

DUODENAL ULCER

Indications for surgery: Patient has to BUY the op

(more complications + duod ulcer will heal provided the high acid secretion of stomach is abolished)

1. Persistent bleeding (e.g. erosion of a post duodenal ulcer into GDA)

2. Perforation
3. Gastric outlet obstruction (patient presents with vomiting of undigested food not long after meal, succussion splash, air-fluid levels on
AXR; characteristic electrolyte abn of hypokalaemic hypochloraemic metabolic alkalosis with paradoxical aciduria)
4. Failure of medical management (ulcer does not heal)

Surgery:

1. Bleed =
a. Duodenotomy + Oversewing/Under-running the bleeding vessel
b. Antiulcer surgery (if patient stable and known case of rebleed/perf)
2. Perforation =
a. Omental patch repair + Bx (small <2cm ulcer / patient unstable)
b. Antiulcer Sx (>2cm or suspect malignancy)
(parietal peritoneum, jejunum serosa, stomach local flap)
3. Definitiveantiulcer surgery
= Duodenectomy + Vagotomy with gastric drainage procedures
- Usually done in elective setting for chronic duodenal ulcers
- Rationale for vagotomy is to eliminate direct cholinergic stimulation to gastric secretion; parietal cells also become less
responsive to histamine and gastrin, and vagal stimulus for gastrin release is abolished
- Vagotomy can be truncal, selective, or highly selective (selecting only those branches that appear to supply peptic cells. does
not require drainage as the Nerves of latarjet that supply the pyloric sphincter are not affected)
- Drainage procedures pyloroplasty (first) or gastrojejunostomy
Usually done with vagotomy as gastric emptying is decreased with denervation.
Pyloroplasty = incise pylorus longitudinally through mucosal layer then suture the incision transversely

Perforated ulcer: IV fluids, IV antibiotics, PPI, surgery (patch repair)

GASTRIC ULCER

Indications for surgery SELL the operation to the patient

(risk of malignancy if >2years)

1. Failure to heal after 3 months of conservative therapy

2. Dysplasia or carcinoma
3. Recurrence
4. Perforation, persistent bleeding

Surgery
1. Bleed =
a. Ulcerectomy (if patient unstable, old, unfit)
b. Antiulcer surgery (if patient stable, can tolerate)
2. Perforation =
a. Omental patch repair + Bx (small <2cm ulcer / patient unstable)
b. Antiulcer Sx (>2cm or suspect malignancy)
(parietal peritoneum, jejunum serosa, stomach local flap)
3. Definitive antiulcer surgery = Gastrectomy
a. Partial gastrec if distal ulcer
b. Proximal ulcers may require total gastrec
Can be used in emergency bleed if patient stable, but considered antiulcer Sx as parietal cell mass and antrum (contains
gastrin containing cells) are removed.
Bancrofts closure (for severe inflammation/scarring that prevents dissection around pylorus. Remove all antral mucosa to
prevent marginal ulcers)

If prepyloric ulcer, can treat similar to duodenal ulcer

4. GASTRIC CANCER

EPIDEMIOLOGY
- Fourth most common cancer in males, sixth most common in females in Singapore
- Female to male ratio 2:1
- Incidence 10-18 per 100,000 per year
- Incidence increases steeply after 50 years old

RISK FACTORS

1. Environmental
- Diet: preserved foods (nitrosamines), smoked foods, polycyclic hydrocarbons
- Smoking
- Alcohol
- Occupational exposure: asbestos, heavy metals, rubber
- Low socioeconomic status

2. Genetic
- Blood type A
- HNPCC Lynch syndrome II
- P53 mutation
- Germline mutation of e-cadherin
- Family history of gastric cancer

PRECURSOR CONDITIONS

1. Partial gastrectomy for benign disease with Bilroth II reconstruction

- Usually occurs >15 years after surgery
- Due to chronic exposure of gastric mucosa to biliary, pancreatic and intestinal secretions at the anastomotic zone

2. Gastric polyps
- Highest risk in inflammatory polyps: 75-90%
- 10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those with villous histology
- Also increased risk of adenocarcinoma elsewhere in the stomach

3. Chronic atrophic gastritis

- Hypertrophic gastritis (Menetriers disease) inflammatory disease of gastric epithelium, up to 10% risk of malignant change
- Pernicious anaemia autoantibodies to parietal cells with achlorhydria, 2-10% risk of gastric cancer

4. Peptic ulcer disease

- <1% risk of malignant change

5. H. pylori infection
- 3-6X increased risk of gastric cancer

HISTOLOGY

a) Adenocarcinomas

- Make up 90-95% of stomach tumours

- Lauren classification:
(a) Intestinal type (most common overall) occurs in high risk population, distal third of the stomach, in older men; associated with erbB2
and erbB3 receptor stimulation
(b) Diffuse type occurs in low risk population, proximal third and cardio-oesophageal junction, in younger and female patients; more
aggressive, present later, worse prognosis; associated with K-sam oncogene

- Early gastric cancer

Confined to mucosa and submucosa
Good survival and prognosis regardless of size, lymph node status, histological grade

b) Non-adenocarcinoma

- Make up less than 10% of stomach tumours

- Types: SCC, neuroendocrine tumour, leiomyosarcoma, GIST (gastrointestinal stromal tumor), primary gastric non-Hodgkins lymphoma
(MALT, linitis plastica) NHL in submucosa adynamic stomach N/V more than anemia
MORPHOLOGY

Borrmanns classification:

Type I (3%): Nonulcerated, polypoid, growing intraluminally

Type II (18%): Ulcerated, circumscribed with sharp margins
Type III (16%): Ulcerated, margin not sharply circumscribed
Type IV (63%): Diffuse, infiltrating, may be ulcerated; may diffuse entire
stomach (linitis plastica)

LOCATION

- 37% in cardia
- 30% in pyloric channel or antrum
- 20% in body
- 12% in entire stomach

SPREAD

- Direct extension to neighbouring organs

- Lymphatic spread
(a) Regional nodes
(b) Supraclavicular nodes (Virchows node)
(c) Umbilical (Sister Josephs node)

- Haematogenous spread liver, lung, bone, brain

- Peritoneal seeding to omentum, parietal peritoneum, ovaries (Krukenbergs tumour), or cul-de-sac / pouch of douglas
(Blumers shelf = shelf-like tumor of ant rectal wall DDx tuberculous peritonitis)

PRESENTATION

Very non-specific symptoms and signs:

- Abdominal pain (usu late)60% 1. Asymptomatic: from histology of ulcer biopsy
- Weight loss 50% 2. Symptomatic: non specific abdominal pain, early
- Nausea/vomiting 40% satiety, N/V, LOW, LOA
- Anaemia 40% 3. Complications: s/s of anaemia, s/s of UBGIT, s/s of
- Palpable mass 30% GOO, s/s of metastasis, peritonism (perforation)
- Haematemesis/malaena 25%
- Early satiety 17%
- Metastatic symptoms late (bony tenderness, neurological deficits, etc)

New onset dyspepsia at age>35 years old should cause concern

COMPLICATIONS

- Bleeding
- Gastric outlet obstruction vomiting (dehydration, hypokalaemic metabolic alkalosis, aspiration pneumonia)
- Perforation
- Malnutrition
INVESTIGATIONS

Diagnosis
OGD visualisation and biopsy (ulcer with heaped-up edges)

Staging investigations
1. CXR/ CT thorax lung mets
2. Endoscopic ultrasound gold standard for T staging and good for N staging
3. CT abdo pelvis good for T, N & M staging
4. Staging laparoscopy prior to operation picks up small peritoneal metastases that are occult on CT scanning (up to 1/5 of
patients) upstage of disease

Complications
5. FBC low Hb
6. U/E/Cr if vomiting, low potassium, low chloride, alkalosis
7. LFTs albumin as a marker of nutritional status (alb<35 is poor); liver mets

STAGING

Tis Carcinoma in situ N0 No regional LN

T1 Tumour limited to mucosa and submucosa N1 1-6 regional LN involved
T2 Tumour invades muscularis mucosa N2 7-15 regional LN involved
T3 Tumour penetrates serosa N3 >15 regional LN involved
T4 Tumour invades adjacent structures

CURATIVE TREATMENT

SURGERY

Principles of surgery:
- Wide resection of the tumour to negative margins (at least 6cm margins)
- En-bloc excision of regional lymph nodes
- Choice between total gastrectomy and subtotal gastrectomy
Subtotal gastrectomy leaves a small portion of proximal stomach easier to anastomose to jejunum than oesophagus since
oesophagus does not have serosa (higher risk of leak)
Subtotal gastrectomy is associated with less morbidity, better functional outcome (some residual reservoir fx preserved)
Total gastrectomy is the resection of choice for proximal tumours (fundus, cardia, body) as well as diffuse-type tumours and
cardio-oesophageal junction tumours

- Reconstruction
Bilroth I (end-to-end gastroduodenostomy) rarely done (diff to mobilise duodenum to anastomose with residual stomach)
Bilroth II/ Poly-A (gastrojejunostomy) no protection against biliary reflux into stomach
Roux-en-Y to prevent biliary reflux; but involves 2 anastomoses, higher chance of leak
Oesophagojejunostomy (after total gastrectomy)
Complications of gastrectomy:

Early
1. Bleeding
2. Infection
3. Anastomotic leak
4. Injury to surrounding structures eg. pancreas

Late

1. Early satiety

2. Retained antrum syndrome

a. Not enough antrum removed acidity in residual stomach, with formation of marginal ulcers on the jejunal side of the anastomosis

3. Intestinal hurry
a. Inadequate reservoir function leads to poor digestion may have phytobezoar (veg fibre bezoar) formation

4. Dumping syndromes
a. Early dumping syndrome (1/2-1hr after meal): due to increased osmotic load from stomach into small intestine flushing, palpitations,
dizziness, nausea, diarrhoea, hypovolemia (due to rapid entry of water into small intestine)
Treat by eating small frequent meals with low carbo and high protein/fat.
b. Late dumping syndrome (1-3hr later): reactive hyperinsulinaemia alimentary hypoglycaemia (weak, sweat, dizzy).
Treat by eating more carbohydrates.

5. Biliary/intestinal reflux into stomach

a. Leads to symptoms of dyspepsia

6. Afferent limb syndrome

a. Occurs in Bilroth II/Polya reconstruction
b. Mechanical obstruction of the afferent jejunal loop due to kinking, anastomotic narrowing, or adhesions postprandial epigastric pain
with nausea, non-bilious vomiting
c. one of the main causes of duodenal stump blowout in the early postoperative period and is also an etiology for postoperative obstructive
jaundice, ascending cholangitis, and pancreatitis due to transmission of high pressures back to the biliopancreatic ductal system
d. Can be decreased by doing Roux-en-Y surgery (but may still occur)

7. Nutritional deficiency
a. Iron deficiency mixed picture
i. Loss of intrinsic factor B12 deficiency
ii. Decreased conversion of iron from Fe3+ to Fe2+ by gastric acid decreased iron absorption in terminal ileum
b. Need to supplement with B12 injections and iron supplements

Post-gastrectomy weight loss

10-33% of pre-op weight
due to LOA (less frequent meals) + decreased reservoir capacity of stomach

Follow-up
- 2/52-1/12: repeat OGD
- 6/12: detect local recurrence (esp if margin involved), check for B12 deficiency
- 1-2 yr: yearly OGD

CHEMOTHERAPY/RADIOTHERAPY

Adjuvant therapy
5-fluorouracil with chemotherapy
5-fluorouracil with epirubicin for advanced disease

Neoadjuvant therapy
- 5-FU and cisplatin can be used to downstage unresectable, locally advanced disease with a significant increase in resectability (61% 79%)
- For resectable disease: preoperative 5-FU, cisplatin, doxorubicin, methotrexate, followed by intraperitoneal 5-FU
improved resection rates, response rates, median survival

PALLIATIVE THERAPY
- For palliation of symptoms such as pain, bleeding, obstruction

1. Endoscopic laser ablation for obstruction

2. Embolisation for bleeding
3. Surgical options: subtotal gastrectomy (6-15% mortality), total gastrectomy (20-40%), gastrojejunostomy for obstruction
4. External beam radiotherapy for pain, low-level ongoing bleeding (not for heavy bleeding as it takes weeks to cause fibrosis)

PROGNOSIS

- Stage I 90% 5-year survival

- Stage II 70%
- Stage III 40%
- Stage IV 0%