Stomach

By Dr Mohammed Abdelrazik
Learning objectives
• By the end of this lectures you should know :
• Principals of Stomach surgical anatomy, physiology, pathology
• Congenital Hypertrophic Pyloric Stenosis
• Cong. Duodenal atresia
• Peptic ulcer disease. Clinical pic, medical and surgical treatment
• Complications of peptic ulcer disease and surgery
 Congenital Hypertrophic Pyloric Stenosis
• Etiology
• The etiology is unknown,
• Genetic and environmental factors.
• Have a familial tendency;
• 80% of cases occur in male infants;
• 50% are first born;
• Associated with macrolide antibiotics (e.g.
Erythromycin) to the
• Mother in late pregnancy
• Or to the infant in the first 2 weeks of life.
Clinical features
• The child usually presents at:
• 3–4 weeks of age,
• Rarely, at or soon after birth.
• Extremely uncommon after 12 weeks.
• The presenting symptom is :
• Projectile vomiting.
• Never contains bile
• The child is always hungry.
• There is failure to gain weight
• Dehydration, constipated
• (The stools resembling the fecal pellets of a rabbit).
• Visible peristalsis of the dilated stomach may be seen in the epigastrium.
• 95% of infants have a palpable pyloric tumor,
• Felt as a firm ‘bobbin’
• In the right upper abdomen,
• Especially after vomiting a feed.
Differential diagnosis

• Enteritis: diarrhea accompanies this.

• Neonatal intestinal obstruction
from duodenalatresia, volvulus neonatorum or intestinal atresia:
symptoms commence within a day or two of birth
and the vomit contains bile.
• Intracranial birth injury.
• Overfeeding
Special investigations
• Ultrasound scan
• thickened and
• elongated pylorus and large stomach.
• • Abdominal X-ray reveals
• a dilated stomach with
• minimal gas in the bowel,
• in contrast to dilated coils of bowel in intestinal obstruction.
• • Barium meal reveals
• characteristic shouldering of the pyloric antrum
• are not usually necessary.
Treatment
• Dehydrated child
• A day or two must be spent in gastric lavage and fluid replacement
(saline with added potassium chloride),
• Healthy child
• Can be submitted to operation soon after admission.
Surgical treatment
Ramstedt’s pyloromyotomy

• A longitudinal incision is made through

the hypertrophied
• Muscle of the pylorus down to mucosa
and the cut edges are separated this
is now commonly performed
laparoscopically. Results are excellent
and the mortality is extremely low.
Duodenal atresia
• Duodenal atresia may be
• Partial
• Complete,
• Affects the second part of the duodenum
• Near the ampulla of vater.
• An annular pancreas may be present
Clinical features
• Antenatal,
• Presence of polyhydramnios and ultrasound appearances.
• Postnatal
• vomiting
• Occurs from birth and the stomach may be visibly distended.
• As the common bile duct usually enters above the obstruction,
• The vomit usually contains bile.
• There is a strong association between
• duodenal Atresia and down’s syndrome,
• 30% of neonates with duodenal atresia having trisomy 21.
 Differential diagnosis
• Esophageal atresia:
• There is choking rather than vomiting.
• Pyloric stenosis:
• Bile is absent from the vomit,
• There is a palpable pyloric tumor
• Onset is later.
• Congenital intestinal obstruction:
• abdominal distension
• X-rays show multiple distended loops of bowel with
fluid levels.
• Plain X-ray of the abdomen is diagnostic and
shows
• Distension of the stomach and proximal duodenum
• With absence of gas throughout the rest of the bowel
• (The ‘double bubble’ sign).
(The ‘double bubble’ sign).
Peptic Ulcer Disease
Anatomy and Physiology of GI Tract
Peptic Ulcers

 Defined
 Ulcerated lesion in the mucosa of the
stomach or duodenum
 Types
 Gastric
 Duodenal
Peptic Ulcer Disease
Stomach Defense Systems
 Mucous layer
 Coats and lines the stomach
 First line of defense
 Bicarbonate
 Neutralizes acid
 Prostaglandins
 Hormone-like substances that keep blood vessels
dilated for good blood flow
 Thought to stimulate mucus and bicarbonate
production
Risk Factors
 Lifestyle  Gender
 Smoking 
Duodenal: are increasing
 Acidic drinks in older women
 Medications 
Genetic factors

More likely if family
 H. Pylori infection member has Hx


90% have this bacterium Other factors:

Passed from person to stress
person (fecal-oral route can worsen but
or oral-oral route)
 Age not the
 Duodenal 30-50 cause
 Gastric over 60
Gastric Ulcers

 Pain occurs 1-2 hours after meals

 Pain usually does not wake patient
 Accentuated by ingestion of food
 Risk for malignancy
 Deep and penetrating and usually
occur on the lesser curvature of
the stomach
Gastric and Duodenal Ulcers
Duodenal Ulcers

 Pain occurs 2-4 hours after meals

 Pain wakes up patient
 Pain relieved by food
 Very little risk for malignancy
General Peptic Ulcer
Symptoms

 Epigastric tenderness
 Gastric: epigastrium; left of midline
 Duodenal: mid to right of epigastrium
 Sharp, burning, aching, gnawing pain
 Dyspepsia (indigestion)
 Nausea/vomiting
 Belching
Complications
Complications of of
Peptic Ulcer
Peptic Ulcers
 Hemorrhage
 Blood vessels damaged as ulcer erodes into the muscles of
stomach or duodenal wall
 Coffee ground vomitus or occult blood in tarry stools
 Perforation
 An ulcer can erode through the entire wall
 Bacteria and partially digested fool spill into
peritoneum=peritonitis
 Narrowing and obstruction (pyloric)
 Swelling and scarring can cause obstruction of food leaving
stomach=repeated vomiting
Diagnostic Tests
 Esophagogastrodeuodenoscopy (EGD)
 Endoscopic procedure
 Visualizes ulcer crater
 Ability to take tissue biopsy to R/O cancer and diagnose
H. pylori
 Upper gastrointestinal series (UGI)

Barium swallow
 X-ray that visualizes structures of the upper GI

 tract
Urea Breath Testing
 Used to detect [Link]

 Client drinks a carbon-enriched urea solution

 Excreted carbon dioxide is then measured

Etiology and Genetic Risk
 PUD primarily associated with NSAID use and
infection with H. Pylori
 Certain drugs may contribute to cause:

 Caffeine – stimulates hydrochloric acid production

 Corticosterioids – associated with an increased
incidence of PUD
 Genetic factors
Drug Therapy/Primary Goals
 Provide pain relief
 Antacids and mucosa protectors
 Eradicate H. pylori infection
 Two antibiotics and one acid suppressor
 Heal ulcer
 Eradicate infection
 Protect until ulcer heals
 Prevent recurrence
 Decrease high acid stimulating foods in susceptible people
 Avoid use of potential ulcer causing drugs
 Stop smoking
Hyposecretory Drugs
 Proton Pump Inhibitors  Prostaglandin Analogs
 Suppress acid production 
Reduce gastric acid and
 Prilosec, Prevacid enhances mucosal
 H2-Receptor Antagonists resistance to injury

 Block histamine-stimulated Cytotec
gastric secretions  Mucosal barrier fortifiers
 Zantac, Pepcid, Axid  Forms a protective coat
 Antacids 
Carafate/Sucralfate
 Neutralizes acid and
 cytoprotective
prevents formation of
pepsin (Maalox,
 Mylanta)
Give 2 hours after meals
and at bedtime
Surgery
 Greatly decreased in the last 20-30 years
secondary to the discovery of H. pylori
 Required if ulcer in one of these states
 Perforated and overflowed into the abdomen
 Scarred or swelled so that there is
 obstruction
 Acute bleeding
Non-responsive to medications
Types of Surgical Procedures
 Gastroenterostomy
allows regurgitation of
alkaline duodenal
contents into the
stomach
 Creates a passage
between the body of
stomach to small
intestines
 Keeps acid away from
ulcerated area
Types of Surgical Procedures
 Vagotomy
 Cuts vagus nerve
 Eliminates acid-
secretion stimulus
Surgical
Procedure/Pyloroplasty
 Pyloroplasty
 Widens the pylorus
to guarantee
stomach emptying
even without vagus
nerve stimulation
Types of Surgical Procedures
 Antrectomy/ Subtotal Gastrectomy

Lower half of stomach (antrum) makes most of
the acid

Removing this portion (antrectomy) decreases
acid production
 Subtotal gastrectomy
 Removes ½ to 2/3 of stomach

Remainder must be reattached to the rest of
the bowel
 Billroth I
 Billroth II
Billroth I
 Distal portion of the
stomach is removed
 The remainder is
anastomosed to the
duodenum
Billroth II
 The lower portion
of the stomach is
removed and the
remainder is
anastomosed to
the jejunum
Postoperative Care

 NG tube – care and management

 Monitor for post-operative complications
Post-op Complications
 Bleeding  Dumping Syndrome
 Occurs at the anastomosed site
 First 24 hours and post-op days 
Prevalent with sub total
4-7 gastrectomies
 Duodenal stump leak 
Early-30 minutes after meals

 Billroth II Vertigo, tachycardia, syncope,
 Severe abdominal pain  sweating, pallor, palpatations

Bile stained drainage on Late – 90 min-3 hours after meals
dressing  Anemia
 Gastric retention 
Rapid gastric empyting

WILL NEED TO PUT NG TUBE
decreases absorption of iron
BACK IN 
Malabsorption of fat

Decreased acid secretions,
decreased pancreatic
secretions, increased upper GI
mobility
Dumping Syndrome

Rapid emptying of food and fluids from the
stomach into the jejunum

Symptoms
 Weakness
 Faintness
 Palpatations
 Fullness
 Discomfort
 Nausea
 diarrhea
Minimize Dumping Syndrome

 Decrease CHO intake

 Eat slowly
 Avoid fluids during meals
 Increase fat
 Eat small, frequent meals