STOMACH AND DUODENUM
3. Intestinal phase
- In this phase the presence of food in the upper portion of the small intestine particularly in the duodenum cause secretion of small amounts of gastric juice in the stomach because of small amounts of gastrin released by the duodenal mucosa.
Clinical correlation
Drugs affecting gastric acid production and secretion:
y H2 blockers: Reversible block of histamine H2-receptors, decrease H+ secretion by parietal cells
y Proton pump inhibitors: Irreversibly inhibit H+/K+ ATPase in stomach parietal cells y Misoprostol: A PGE1 analogue. Increase the production and secretion of gastric mucous
barrier.
Q11. Enumerate the causes of gastric outlet obstruction.
Describe the pathophysiology of gastric outlet obstruction and discuss the fluid and electrolyte abnormalities in a patient with gastric outlet obstruction.
Ans. Gastric outlet obstruction is a clinicopathological entity resulting from any disease or disorder that leads to a mechanical or non-mechanical impairment in gastric emptying function.
Causes are as shown in the flow chart below:
Clinical Presentation
y Vomiting is the principal symptom with undigested food particles and nonbilious nature of vomitus usually within 1 to 2 hrs of food intake
y Progressive weight loss and malnutrition
y Early satiety, bloating, anorexia, epigastric fullness are other symptoms
y On examination, patient may be dehydrated and malnourished with presence of a tympanitic mass in the epigastrium and left hypochondrium with presence of succussion splash.
Metabolic complications of gastric outlet obstruction Pathophysiology
y Loss of acid in gastric vomiting lead to hypochloremic metabolic alkalosis
y Initially H+ is exchanged for Na+ and K+ in distal tubules of kidney to conserve H+. Therefore, the urine initially is alkaline with resultant hypokalemic, hyponatremic, hypochloremic metabolic alkalosis
y In longstanding cases, due to prolonged and severe hypochloremia, kidney starts conserving chloride ions which are absorbed along with Na+ ions which lead to loss of potassium and hydrogen ions in urine thus resulting in paradoxical aciduria
y Thus, paradoxical aciduria is a consequence of renal attempt to correct hypochloremia
y So final result is hypokalemic, hyponatremic, hypochloremic metabolic alkalosis with paradoxical aciduria.
Diagnoses
y Sodium chloride load test: First nasogastric tube is inserted and contents aspirated.
If contents greater in amount then no need to perform the test. Otherwise, to confirm GOO, 750 ml of isotonic saline is instilled into stomach via nasogastric tube and effluent is checked. If volume > 400ml is aspirated at 30 minutes after instillation, the test is positive y Nuclear gastric emptying studies, barium upper GI studies, Upper GI endoscopy
can also be used as indicated
y CECT abdomen can also aid in diagnoses especially when periampullary or pancreatic pathology is suspected.
Management
y Nasogastric tube is inserted to decompress the stomach and GI fluid loss is replaced ml for ml
y Percutaneous jejunostomy can be done for feeding purpose if long standing GOO y This condition is more a medical emergency than a surgical emergency where patient
presents with fluid and electrolyte abnormalities
y Correct the abnormality with 0.45% saline and 5% glucose at 150 to 175 ml/kg/day with 2 to 4 meq/kg potassium added to the fluid for the initial 24 hours
y Maintain a urine output of >1 ml/kg/hr
y Serum bicarbonate also needs normalization before proceeding to surgery for correction of cause
y Post operative IV fluids should be continued for several hours followed by oral intake as tolerated.
The surgical management depends on correction of the underlying condition that is causing GOO.
Q12. Write a note on congenital hypertrophic pyloric stenosis.
Mention the fluid and electrolyte abnormalities in congenital hypertrophic pyloric stenosis – same as in gastric outlet obstruction.
Ans. A condition characterized by:
y Mechanical obstruction of gastric outlet due to hypertrophy of the circular muscle layer of the pylorus of the stomach
y The pyloric canal lengthens, the whole pylorus thickens and the mucosa becomes oedematous causing functional obstruction of the gastric outlet.
Clinical presentation:
y Incidence : 1 in 4000 live births
y First born males are the more commonly affected infants y High risk in offsprings of parents with this condition.
Symptoms
y Vomiting is the first symptom in most children
– May occur after every feeding or only after some feedings.
– Usually starts around 3 weeks of age, but may start any time between 1 week and 5 months of age.
– Forceful (projectile vomiting)
– The infant is hungry after vomiting and wants to feed again.
Other symptoms generally appear several weeks after birth and may include:
y Dehydration gets worse with the severity of the vomiting. Prolonged vomiting leads to the loss of large quantities of gastric secretions rich in H+ and Cl–.
y As a result of dehydration, the kidney attempts to conserve Na+ to maintain volume, by exchanging them for K+ and H+(paradoxical aciduria).
y Starvation can exacerbate diminished hepatic glucoronyl transferase activity, and indirect hyperbilirubinemia may be seen in 1–2% of affected infants.
y Failure to gain weight or weight loss.
y Wave-like motion of the abdomen shortly after feeding and just before vomiting occurs.
Etiology
y It has been found in IHPS specimens that the muscle layer is deficient in:
– The quantity of nerve terminals – Markers for nerve-supporting cells – Peptide-containing nerve fibers
y This abnormal innervation of the muscular layer leads to failure of relaxation of the pyloric muscle, increased synthesis of growth factors and subsequent hypertrophy, hyperplasia and obstruction
y There is an increased incidence of IHPS in infants receiving erythromycin. The reason is unclear, although a prokinetic effect on gastric muscle contraction is postulated.
Diagnosis
y Initially suggested by the typical clinical presentation
In physical examination : The mass is firm, mobile, approximately 2 cm, best palpated from the left, located in the midepigasrtrium beneath the liver edge
y Palpation of the hard muscle mass or olive is diagnostic in conjunction with a typical history.
y Diagnosis by palpation of olive have only 49% successful of cases in recent years compared with 78% successful cases 30 years ago.
y Ultrasonography is used to measure the thickness of the pyloric wall and the length of the pyloric canal.
– normal wall thickness < 2 mm, IHPS > 4 mm
– normal length of the pyloric canal < 10 mm, IHPS > 15 mm and – outer wall to wall diameter > 15 mm
y Sensitivity and specificity as high as 100%
y Signs on barium meal – String sign, shoulder sign and double- track sign.
Differential Diagnoses y Gastroesophageal reflux y Adrenal insufficiency y Viral gastroenteritis
Treatment
The preoperative treatment is directed toward correcting the fluid, acid-base and electrolyte.
Losses as CHPS like GOO is more a medical emergency.
y Intravenous fluid therapy is begun with 0.45 to 0.9% saline, in 5 to 10% dextrose with the addition of potassium chloride in concentrations of 30 to 50 mEq/L
y Fluid therapy should be continued until the infant is rehydrated and the serum bicarbonate concentration is less than 30 mEq/dL, which implies that the alkalosis has been corrected
y Most infants can be rehydrated within 24 hours.
Surgical management
y Once resuscitated the infant can undergo the Fredet-Ramstedt pylormyotomy, which is the procedure of choice
y It consist of incision in to the sphincter muscle of pylorus
y NG tube is passed and gastric content are aspirated just prior to surgery.
Complications
y Wound infection, mucosal perforation at duodenal end and incomplete myotomy.
Q13. Discuss the role of H. pylori in pathogenesis and management of peptic ulcer disease.
Ans.
Helicobacter pylori Infection
y Warren and Marshall were the first to identify and isolate the organism.
y 90% of duodenal ulcers and roughly 75% of gastric ulcers are associated with H. pylori infection.
Organism characteristics
y It is a spiral or helical gram-negative rod with 4 to 6 flagella.
y It is microaerophilic and the optimal temperature for isolation is 35°C to 37°C with growth occurring after 2 to 5 days.
y It resides in gastric-type epithelium because only this epithelium expresses the necessary adherence receptors for the H. pylori to attach and reside within or beneath the mucus layer which protects it from both acid and antibiotics.
y It is one of the most potent producers of urease which splits urea into ammonia and bicarbonate creating an alkaline microenvironment in the setting of an acidic gastric milieu. It also produces catalase and oxidase.
y It can also be found in heterotopic gastric mucosa in proximal esophagus and Barrett’s esophagus, in gastric metaplasia in the duodenum and Meckel’s diverticulum and in heterotopic gastric mucosa in the rectum.
y It can be grown in chocolate medium and skirrow’s medium.
Mode of infection
y Infection is more common in developing countries, has familial clustering and occurs through contaminated food and water
y A person once infected will never show spontaneous remission, and once treated will show eradication of the organism and no ulcer recurrence.
Mechanism of injury
y The mechanisms responsible for H. pylori–induced GI injury remain to be fully elucidated, but three potential mechanisms have been proposed:
– Production of toxic products (ammonia, cytotoxins, mucinase and phospholipase) to cause local tissue injury
– Induction of a local mucosal immune response
– Increased gastrin levels with a resultant increase in acid secretion. The toxic produts cause mucosal injury and thrombosis in the microcirculation
y H. pylori is known to cause a local inflammatory reaction in the gastric mucosa and to produce chemotactic factors that attract neutrophils and monocytes. Activated monocytes and neutrophils in turn, produce a number of proinflammatory cytokines and reactive oxygen metabolites
y Reduction in antral D cells and decreased somatostatin caused by infection with H. Pylori also predispose to ulceration.
Diagnostic methods Noninvasive Techniques
y Blood test: Serology. Not useful to document eradication
y Urea breath test: The patient swallows a capsule, liquid or pudding that contains urea
“labeled” with a special carbon atom. After a few minutes, the patient breathes into a container, exhaling carbon dioxide. If the carbon atom is found in the exhaled breath, H. pylori is present, as this bacterium contains large amounts of urease, a chemical that breaks urea down into carbon dioxide and ammonia.
y Stool antigen test: The patient provides a stool sample, which is tested for H. pylori antigens.
Invasive Techniques
y UGI endoscopy and biopsy based tests
Rapid urease test/histology (warthin starry silver stain, giemsa stain)/culture can all be done on the sample.
Diseases associated with H. pylori infection y Duodenal ulcer
y MALT lymphoma
y Antral gastritis/ Chronic atrophic gastritis/Nonatrophic pangastritis y Gastric adenocarcinoma
y Gastric ulcer
y Carcinoma pancreas, gallbladder, squamous cell cancer esophagus y Menetrier’s disease.
Management implications
y All patients are given anti-H. pylori medications as the standard triple drug therapy [lansoprazole/omeprazole + metronidazole + clarithromycin (LCM)] for 14 days with urea breath test as the best follow up test to document eradication
y Also patients with low grade MALT lymphoma are prescribed the anti-H. pylori medication and response is evaluated. This might be the only treatment required in these cases y Recurrence of peptic ulcer without this medical management is in the range of 60 to
70% which is decreased to less than 10 to 20% with the medical management.
Q14. Classify Peptic ulcers. Give the surgical options for management of peptic ulcers.
Enumerate the complications of the peptic ulcers and discuss its management in brief.
Discuss the management of a patient with perforated peptic ulcer.
Ans. Modified Johnson Peptic ulcer classification
Type Location Acid level Vagotomy
1 Lesser curvature (m.c.) Low No role
2 Body of stomach and duodenum High Useful
3 Prepyloric antrum High Useful
4 High on lesser curvature, near GEJ Low No role
5 Anywhere but medication induced Low No role
Features and complications
Gastric ulcer Duodenal ulcer
1. Pain after taking food and relieved by vomiting
2. Hemetemesis common 3. Loss of weight seen
4. Spoke wheel pattern/hampton’s line/
penetrating sign/preserved peristalsis seen in benign gastric ulcer
1. Pain on empty stomach and relieved after eating
2. Melena common 3. Weight gain seen
4. Trifoliate duodenum or absent duodenal cap seen on barium study
Complications
5. Perforation into lesser sac is the most common complication
6. Malignant transformation can occur 7. Gastric outlet obstruction can occur
5. Bleeding of gastroduodenal artery erosion into posterior wall is most common 6. Never occurs
7. Gastric outlet obstruction can occur 8. Perforation occurs in anterior wall
Surgical options for peptic ulcer patients
Indications have diminished since the advent of H. pylori therapy.
Goal – Decrease acid secretion from stomach.
Options
y Remove vagal stimulation via vagotomy
y Remove gastrin-driven secretion by performing an antrectomy
y Vagotomy with antrectomy is additive and decreases acid output by 85%.
Procedures
Vagotomy Drainage (done with
truncal vagotomy) Resection and
reconstruction Type 4 gastric ulcer Truncal vagotomy
(above celiac and hepatic branch)
Pyloroplasty y Heinke Mikulicz y Finney
y Jaboulay
y Weinberg modification of Heinke Mickulicz
Subtotal
gastrectomy Kelling Madlener procedure for unstable patients
Selective vagotomy (below celiac and hepatic branch)
Gastroduodenostomy
(Billroth 1) Antrectomy Csendes procedure
for stable patients
Highly selective
vagotomy Gastrojejunostomy
(Billroth 2) Pouchet procedure
Hill baker procedure Braun gastrojejunostomy Shoemaker procedure Taylor procedure Roux–en–y uncut GJ
Truncal Vagotomy
y Performed by division of the left and right vagus nerves above the hepatic and celiac branches just above the GE junction
y Some form of drainage procedure is used in association with truncal vagotomy y Bile reflux may be more common after gastroenterostomy and diarrhea is more common
after pyloroplasty. The incidence of dumping is the same for both.
Highly selective vagotomy (Parietal Cell Vagotomy or proximal gastric vagotomy) y Divides only the vagus nerves supplying the acid-producing portion of the stomach
within the corpus and fundus and preserves the vagal innervation of the gastric antrum so that there is no need for routine drainage procedures
y The criminal nerve of Grassi represents a very proximal branch of the posterior trunk of the vagus and great attention needs to be taken to avoid missing this branch in the division process as it can lead to ulcer recurrence if left intact.
Truncal Vagotomy and Antrectomy
y Antrectomy requires reconstruction of GI continuity that can be accomplished by a gastroduodenostomy (Billroth I procedure) or gastrojejunostomy (Billroth II procedure) or polya gastrectomy or Roux-en-Y gastrojejunostomy
y The retrocolic anastomosis minimizes the length of the afferent limb and decreases the likelihood of twisting or kinking that could lead to afferent loop obstruction.
Operation Mortality (%) Side effects (%) Recurrence (%)
Vagotomy and antrectomy 2 5 1
Vagotomy and drainage 1 5 10
Highly selective vagotomy 0.2 1 10
Gastric ulcers
Elective/Intractable cases Type 1 Distal gastrectomy and reconstuction Type 2 and 3 Truncal vagotomy and antrectomy
Type 4 As mentioned above
Perforation Stable
Unstable As above
Patch closure after biopsy
Bleeding Stable
Unstable As above
Oversew and biopsy
Obstruction Stable
Unstable As above
Bypass and biopsy
Duodenal Ulcers
Perforation Stable
Unstable Patch repair with truncal vagotomy (TV) patch closure
Intractability Highly selective vagotomy
Bleeding Stable
Unstable TV with pyloroplasty Oversew.
Obstruction Stable
Unstable TV with antrectomy or GJ Bypass
Management of perforated peptic ulcers is now described in the SN as follows:
y Gastric ulcers perforate into lesser sac and duodenal ulcers perforate into pancreas through its anterior wall
y Clinical features of acute abdomen
y Patient present in shock and features of dehydration
y Patient also prefers lying still and has shallow respiration with diffuse abdominal pain and tenderness. Nausea, vomiting are also present
y Important signs: Generalized rebound tenderness/Guarding and obliteration of liver dullness suggest perforation peritonitis
y Investigations: Chest X-ray with both domes of diaphragm show free gas under diaphragm in 80% patients and is the only investigation required for diagnoses.
y Management
– Resuscitation with isotonic fluids with two wide bore IV lines (green canula) – Antibiotics IV
– Nasogastric aspiration, foley’s catheterization and analgesia – Antisecretory agent infusion to be started
– Rule out coagulopathy and monitor urine output and vitals of the patient – Arrange blood and take care of cardiopulmonary status of the patient
y Lastly, write the surgical management options and the management as shown in table y Factors affecting the outcome in patients with peptic ulcer perforation include:
(Mn: DASH)
y Delay from initial diagnoses to treatment y Age of the patient
y Site: Gastric has poorer prognosis
y Hypotension at presentation has a poor prognoses.
Q15. Classify postgastrectomy problems and explain the pathophysiology and management of dumping syndrome.
Ans.
Due to metabolic
problems Gastric reservoir
dysfunction Related to
vagotomy Related to reconstruction Anemia – iron, B12,
Folate deficiency Dumping – early/
late Diarrhea Reflux gastritis
Osteopenia Gallstones Afferent loop syndrome
Weight loss Gastric stasis Efferent loop syndrome
Roux syndrome
Jejunogastric intusussception Retained antrum syndrome
Incidence – 25% and only 1% has permanant disabling symptoms.
Dumping syndrome
Can be early (20 to 30 minutes after eating) or late (2 or 3 hours after a meal).
Early dumping y More common
y More often with Billroth II reconstruction than with Billroth I gastrectomy/ vagotomy and drainage procedures
y Occurs because of the rapid passage of food of high osmolarity from the stomach into the small intestine
y The hypertonic food bolus induces a rapid shift of extracellular fluid into the intestinal lumen to achieve isotonicity
y This causes luminal distention and induces the autonomic responses and release of neurotransmitters like serotonin, neurotensin, bradykinin-like substances
y More GI symptoms and fewer cardiovascular effects
y GI symptoms include nausea and vomiting a sense of epigastric fullness, cramping abdominal pain and often explosive diarrhea
y The cardiovascular symptoms include palpitations, tachycardia, diaphoresis, fainting, dizziness, flushing and occasionally blurred vision.
Late dumping
y Cause is rapid gastric emptying however, specifically to carbohydrates being delivered rapidly into the proximal intestine
y This triggers the release of large amounts of insulin to control the rising blood sugar level y This results in an overcompensation so that a profound hypoglycemia occurs in response
to the insulin
y This activates the adrenal gland to release catecholamines, which results in diaphoresis, tremulousness, light-headedness, tachycardia and confusion.
Management
y Dietary measures are usually sufficient
y Avoiding foods containing large amounts of sugar.
y Frequent feeding of small meals rich in protein and fat.
y Separating liquids from solids during a meal.
y Long-acting octreotide agonists have ameliorated symptoms
y Operative procedures include conversion of Billroth 2 to Billroth 1 or conversion of both to roux-en-y gastrojejunostomy, antiperistaltic jejunal loop placecment to delay transit are some of the options to treat dumping syndrome.
Q16. Discuss the causes of upper GI bleeding. Outline the management of a patient with upper GI bleeding.
Ans.
Upper GI bleed
y Bleeding proximal to ligament of treitz is called upper GI bleed.
Causes
Nonvariceal (80%) Portal hypertensive bleed (20%) Peptic ulcer (50-60%) m.c. Gastroesophageal varices (>90%)
Mallory weiss tear Hypertensive gastropathy
Gastritis/duodenitis Isolated gastric varices Esophagitis
AV malformations Tumors
Angiodysplasia,hemobilia
Management Step 1
y Fluid and electrolyte Resuscitation y Nasogastric decompression
y Rule out coagulopathy, Hematocrit, arrange blood y Start IV antibiotic and infusion of proton pump inhibitors y Rule out use of chronic NSAIDS, alcohol, smoking and steroids.
Step 2
In a stable patient, endoscopy to be done within 24 hours Further management depends on endoscopic findings.