Gastric and duodenal ulcer disease. Anatomy Arterial blood supply Lymphatic drainage Nerve supply.

Gastric and duodenal ulcer Gastric and duodenal ulcer diseasedisease

AnatomyAnatomy Arterial blood supply Lymphatic drainage Nerve supply

PHYSIOLOGYPHYSIOLOGYFunction:

1. Digestion of food, reduce the size of food

2. Acts as reservoir

3. Absorption of Vit. 12, iron and calcium

Stimulant of Gastric secretion:1. Gastrin -----> (+) parietal cell

2. Acetylcholine (vagus) ---> (+) gastric cells

3. Histamine (mast cells) ---> parietal & chief cells

PHYSIOLOGYPHYSIOLOGYBAO: 2 – 5 meq of acid/hr. (vagal tone and basal

histamine secretion)

MAO: 1. Cephalic (vagus) ---> (+) parietal & G cell

10 meq acid/hr.

2. Gastric: ---> (+) vagus & G cell 15 – 25 meq of acid/hr pH = < 2.0

3. Intestinal: Chyme enters the duodenum (-) gastric release Secretin, gastric inhibitory peptide, peptide YY

– ACID condition sterilized the area, except for HELICOBACTER PYLORI

Protective factors Protective factors vs.vs. hostile factors hostile factors

Peptic Ulcer DiseasePeptic Ulcer Disease

PathogenesisPathogenesis : :

Peptic ulcerPeptic ulcerPathogenesis:1. For both Duodenal & Gastric Ulcers:

a. Infection w/ H. pylori: Decreases resistance of mucus layer from acid

permeation (hydrophobicity)

Increase acid secretion

Slow duodenal emptying

Reduced both duodenal and gastric bicarbonate secretion

Clinical ManifestationClinical Manifestation1. Abdominal pain:

– Due to irritation of afferent nerves w/in the ulcer by the acid or due to peristaltic waves passing through the ulcer

Duodenal: colicky or burning pain relieved w/ food intake

Gastric: gnawing or burning usually during or after eating.

2. N/V

3. Weight loss

4. Epigastric tenderness

Peptic ulcerPeptic ulcerPathogenesis:

b. Effects of NSAIDs Decreases ProstagladinProstaglandin – inhibits acid secretion, stimulates mucus

and HCO3 secretion and mucosal blood flow

c. Zollinger-Ellison Syndrome (1%): Massive secretion of HCL due to ectopic gastrin

production from non-beta islet cell tumor (gastrinoma) Associated w/ type I (MEN) PPP 20% multiple, 2/3 malignant, w/ slow growing Parietal cell mass is increased > gastrin 3-6 x the normal

Symptoms of gastric ulcer disease:

epigastric pain after meal or during meal

upper dyspeptic syndrome – loss of appetite, nauzea, vomiting, flatulence

vomiting brings relief

reduced nutrition

loss of weight

Comparing Duodenal Comparing Duodenal and Gastric Ulcersand Gastric Ulcers

Symptoms of duodenal ulcer disease:

epigastric pain 2 hours after meal or on a empty stomach or during night

pyrosis

good nutrition

obstipation

seasonal dependence (spring, autumn)

Diagnosis:Diagnosis:

1. UGIS (double contrast)

2. Endoscopy

Therapy:

Conservative • regular lifestyle• prohibition of the smoking and alcohol• diet (proteins, milk and milky products)• pharmacology (antagonists of H2 receptors,

antacids, anticholinergics

Surgical • BI, BII resection• proximal selective vagotomy• vagotomy with pyloroplastic• suture of perforated or haemorrhagic ulcer

Stomach Stomach resections:resections:

BillrothBillroth I (BI) I (BI) – – gastro-duodenoanastomosis end-to-endgastro-duodenoanastomosis end-to-end

Billroth II (BII)Billroth II (BII) – gastro-jejunoanastomosis end-to-side – gastro-jejunoanastomosis end-to-side with blind closure of duodenumwith blind closure of duodenum

ProximalProximal selective vagotomyselective vagotomy – denervation – denervation of parietalof parietal gastric cellsgastric cells

Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004

Billroth I

Billroth II



Gastro-enteroanastomosis on Roux Y crankle


Vagotomy

TreatmentTreatment

Primarily medical– PPI or H2 blocker– Triple combination (double antibiotic and PPI=amoxicillin,

clarithromycin, pantoprazole for 7-14 days) Surgical indications

– Intractibility (after medical therapy)– Hemorrhage– Obstruction– Perforation– Relative: continuous requirement of steroid therapy/NSAIDs

Treatment:Treatment:

Mechanism of Pharmacologic Therapy:4. For eradication of H. pylori:

a. Bismuth based triple therapy Bismuth + Tetracycline + Metronidazole

b. Proton pump inhibitor Omeprazole + Amoxicillin/Clarithromycin

+ metronidazole

Treatment:Treatment:

Surgical Treatment:Indication:1. Intractability:

– Highly selective vagotomy Low septic complication, (-) dumping and diarrhea

– For gastric ulcer: Total or subtotal gastrectomy w/ or w/o vagotomy


A – penetration B – perforation

C – bleeding D - stenosis

GI BleedingGI Bleeding

Ulcer with recent bleedUlcer with recent bleed

Treatment:Treatment:Surgical Treatment:

Indication:2. Hemorrhage: s/sx

– Critically ill– Endoscopy– Surgery: a. continue bleeding for more

than 6 units

b. recurrent bleeding after endoscopically controlled

- pyloroduodenostomy + HSV

- pyloroduodenostomy + vagotomy + pyloroplasty

Ulcer Perforation

Treatment:Treatment:Surgical Treatment:

Indication:3. Perforation: S/Sx

Graham omental patch only for shock, perforation > 48 hrs or other medical problem

Vagotomy + pyloroplasty; HSV Vagotomy + Gastrojejunostomy

4. Obstruction: S/Sx; Saline loading test Vagotomy + Antrectomy Vagotomy + Gastroenterostomy

Gastric outlet obstructionGastric outlet obstruction

Elective Surgical TherapyElective Surgical Therapy

Rare; most uncomplicated ulcers heal within 12 weeks

If don’t, change medication, observe addition 12 weeks

Check serum gastrin (antral G-cell hyperplasia or gastrinoma)

EGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory

Modified Johnson Modified Johnson ClassificationClassification

Type Location Acid

HypersecretionI Lesser curvature, incisura No

II Body of stomach, incisura, and duodenal ulcer (active or healed)

Yes

III Prepyloric Yes

IV High on lesser curve, near gastroesophageal junction

No

V Anywhere (medication induced) No


Type I

Type IType I

Lesser curvature; incisura

MOST COMMONDecreased mucosal

protection (no vagotomy)

Distal gastrectomy (INCLUDING UCLER) with BI

Billroth IBillroth I


Type II/III

Type 2/3 UlcersType 2/3 Ulcers

Acid hypersecretion Antrectomy with ulcer and

bilateral truncal vagotomy Billroth II or Billroth I

depending on technical difficulty

Parietal cell vagotomy option but higher recurrence

Billroth IIBillroth II

R-Y limb (subtotal R-Y limb (subtotal gastrectomy)gastrectomy)


Type IV

Type 4 UlcersType 4 Ulcers Least common (5% of all

gastric ulcers) Ulcers 2-5cm from cardia

can be treated with distal gastrectomy, extending resection along the lesser curvature and BI (Pauchet/Shoemaker procedure)

Ulcers closer to GEJ, tongue-shaped resection high onto lesser curve (Csendes’ procedure with Roux-en-Y reconstruction)

Cardia

CSENDES RESECTION (Line of transection; Roux-en-Y anastomosis)


Giant Gastric Ulcer

Giant Gastric UlcerGiant Gastric Ulcer

Giant gastric ulcer: >3cm; 30% malignancy risk

Subtotal gastrectomy with Roux-en-Y (high morbidity and mortality)

Kelling-Madlener procedure: less aggressive, antrectomy, BI reconstruction, bilateral truncal vagotomy, leave ulcer, multiple biopsies, cautery of ulcer

Complications after stomach resection:

Early – dehiscence, stenosis of anastomosis, bleeding, pancreatitis, obstructive icterus, affection of neighbour tissues

Late - days, weeks

- early dumping syndrome

- late dumping syndrome

- incoming crankle syndrome

- outcoming crankle syndrome

- ulcer in anastomosis or in outcoming crankle

Early Complications (1)Early Complications (1)1. Failure of the stomach or stomach remnant to empty occurs after

any procedure. It was formerly common after vagotomy and drainage. Causes are:

A. Prolonged paralysis of stomach (doubtful)

B. Edema at a stoma

C. Fluid and electrolyte disorder, especially hypokalaemia.

Management is conservative with NG suction, fluid, electrolyte and nutritional replacement.

Early Complications (2)Early Complications (2)

2. Intestinal obstruction.

Causes are:

A. Adhesive.

B. As a consequences:

(a) Twisting of the loop of a gastrojejunostomy after polya gastrectomy.

(b) Herniation of loops through a mesenteric defect.

(c) Retrograde intussusception of the efferent loop of a gastrojejunostomy (rare).

Prophylaxis: avoid causes – such as mesenteric cul de sacs or holes

Treatment: operative


3. Fistulae. Can occur after any operation, which involves a suture line. Most usual sites are:

1. After polya gastrectomy i. Duodenal stump ii. Pancreases from trying to dissect

out a difficult ulcer 2. Occasionally at a Pyloroplasty


4. Acute pancreatitis. May follow any procedure. Its etiology is unknown, but some cases are traumatic

Late Complications (1)Late Complications (1)1. Anastomotic and recurrent ulceration Causes: a. Inadequate resection of parietal cell mass.b. Isolated antrum left after polya gastrectomy.c. Zollinger – Ellison syndrome.d. Incomplete vagotmy.e. Persistent suture in the anastomosis. More usually this is merely a suture

exposed as a consequence of ulceration from another cause.

Prophylaxis: adequate primary treatment.

Management is related to cause and requires investigation to ascertain the level of acid secretion or the completeness of vagotomy. Recurrence after vagotomy is best managed by polya gastrectomy.

Late Complications (1)Late Complications (1)2. Gastrojejunocolic fistulae.

Occurs when a recurrent ulcer after gastrojejual anastomosis penetrates into the colon. It should arouse the suspicion of Zollinger-Ellison syndrome.

Clinical features: Severe diarrhea occurs due to enteritis caused by cronic contents passing directly into the small bowel and acidosis, dehydration, potassium loss, anaemia and cachexia will result in death if the fastula is not interrupted surgically.

Treatment:

1. Good risk patient. Excision of the gastric, jejunal and colonic components and the construction of a higher gastrectomy.

2. Poor risk patient. A staged procedure:

(a) Stage 1: Proximal colostomy which, diverts the faecal stream from the fistula and thus stops the enteritis.

(b) Stage 2: Excision of fistula and its visceral components and the construction of a higher gastrectomy and colonic anastomosis.

(c) Stage 3: Closure of colostomy.

Early dumping syndrome:

group of symptoms approved shortly after meal

appears after BII resection

vasomotoric sy. - face redness, fall of blood pressure, dizziness

GI sy. - vomiting, diarrhoea

Th.: diet, no sugar, low quantities of food, change BII to BI resection

LateLate dumping syndrome: dumping syndrome:

hhypoglycaemiaypoglycaemia (sugar is not enough digested)(sugar is not enough digested)

appears after BII resectionappears after BII resection

weakness, perspiration, dizzinessweakness, perspiration, dizziness, , tremor ccatremor cca 3h 3h afterafter mealmeal

Th.:Th.: no sugar, change BII to BI resection no sugar, change BII to BI resection

Anemia Anemia

Partial gastrectomy and polya reconstruction interferes with duodenal absorption of iron and a macrocytic anemia may result

More rarely, sufficient stomach has been removed to cause failure of release of intrinsic factor and thus a macrocytic anemia

Malnutrition may contribute to both.

Weight loss and its complications Weight loss and its complications

Particulary after partial gastrectomy when patients are unwilling to eat sufficiently, weight loss is common

Severe malnutrition is rare, but there is an increased risk of nutrition-associated diseases such as tuberculosis.

Bilious vomiting Bilious vomiting Any operation which, destroys or bypasses the

pylorus allows bile to reach the stomach.Not only does this produce atrophic gastritis but

also it may be associated with bilious vomiting.This is more likely after a polya gastrectomy

where characteristically a patient eats a meal and some to 10 to 20 minutes later vomits bile only.

In severe cases, either normal anatomy should be restored or the bile diverted more distally into the intestine.

DiarrheaDiarrhea

Apart from the dumping syndrome, all vagotomies except highly selective ones seem to cause diarrhea

Matters are made worse if cholecystectomy has been done or is subsequently done

Acute Gastritis (erosive)Acute Gastritis (erosive) Stress erosions are usually multiple, small punctuate

lesion in the proximal acid secreting portion of the stomach

Clinical Settings:1. Severe illness, trauma, burns (Cushing ulcer) or

sepsis– Due to (-) mucosal defense (ischemia)

2. Drug and Chemical ingestion– Aspirin / NSAIDs

3. CNS trauma:– Increase gastrin ---> elevated acid secretion– Curling ulcer

Acute GastritisAcute GastritisPathogenesis:

1. Aspirin, bile salts (backflow), alcohol2. Mucosal ischemia

Clinical manifestations:1. Gastrointestinal bleeding2. Abdominal pain

Diagnosis:– Endoscopy / radionuclide scanning / visceral

angiography

Acute GastritisAcute Gastritis

Treatment:– NPO– NGT / Saline lavage– Antacids / omeprazole / sucralfate– Intra-arterial infusion of vasopressin– Surgery --> if 6-8 units over 24 hrs

Mortality ---> 40%

1. Near total gastrectomy

2. Vagotomy + pyloroplasty + over sewing of bleeder

3. Partial gastrectomy + vagotomy

Zollinger-Ellison Syndrome Zollinger-Ellison Syndrome (Gastrinoma)(Gastrinoma) Symptoms tends to be more severe, unrelenting and less

responsive to therapy.

Clinical Manifestation:1. Pain2. Diarrhea3. Steatorrhea

Diagnosis:1. Acid secreting studies (50meq/hr)2. UGIS3. Radio-immuno assay for serum Gastrin level

Diff: a) Pernicious anemia b) Renal insufficiency c) Antral gastrin hyperplasia or hyperfunction

4. CT scan and angiography to localize gastrinoma5. Venous sampling

Gastric and duodenal ulcer disease. Anatomy Arterial blood supply Lymphatic drainage Nerve supply.

Documents

Transcript of Gastric and duodenal ulcer disease. Anatomy Arterial blood supply Lymphatic drainage Nerve supply.