Gastric Outlet
Obstruction
Presented by 7.8.2024
Cadet Myo Thant Kyaw
Cadet Ya Wai Aung
Contents
• Introduction
• Epidemiology
• Causes
• Pathophysiology
• Investigation
• Treatment
Introduction
• Gastric outlet obstruction (GOO, also known as pyloric obstruction) is
not a single entity
• It is clinical and pathophysiological consequence of an disease process
that produces a mechanical impediment to gastric emptying
Epidemiology
• Until the late 1970s benign disease was responsible for a majority of
cases
• Now, with the decrease in the incidence of PU and the advent of
potent medical treatments, GOO should be considered malignant
until proven otherwise, at least in the WEST
Causes
Common
• Chronic DU with stenosis
• Ca stomach (antrum)
Uncommon
• Luminal
• Mucosal diaphragm – failure of recanalization of embryonic gut
• Bezoars – Tricho (Hair ball) and Phyto (Vegetable ball)
Cont;
• Mural
• Adult pyloric hypertrophy
• Megaduodenum
• Carcinoma or lymphoma
• Duodenal haematoma
• Extraluminal
• Annular pancreas
• Arteriomesenteric compression (Wilkie’s disease or superior mesenteric A syndrome
• Pancreatic pseudocyst
• Ca head of pancreas
Cont;
• Trichobezoar
• It is a hair-ball commonly seen in stomach of females with psychiatric
illness who swallow hair regularly
• It forms a ball like mass occupying the full stomach
• Extending to duodenum and jejunum called Rapunzel syndrome
• Phytobezoar- solid ball formation in the stomach comprising plant
fibers &seeds
Cont;
• Wilkie’s syndrome
• Due to obstruction of the 3rd
part of the duodenum due to
decrease angle between SMA
and aorta
• It can be due to congenital or
traumatic aneurysm of SMA
Cont;
Cont;
Annular pancreas
• A ring of pancreatic tissue that
completely encircles the duodenum
• Pathogenesis
• May occur when the ventral bud splits
(become bifid),the two segments may
encircle the duodenum
Cont;
Pyloric mucosal diaphragm
• The origin of this rare conditional is
unknown
• It usually does not become apparent until
middle age
Adult pyloric stenosis
• This is a rare condition and its relationship
to the childhood condition is unclear
• Some patients have a long H/O problems
with gastric emptying
Pathophysiology
• Intrinsic or extrinsic obstruction of the pyloric channel or duodenum
is the usual P/P of GOO
• The mechanism of obstruction depends upon the underlying etiology
• Patients presented with intermittent symptoms that progress until
obstruction is complete
• Initially, patients may demonstrate better tolerance to liquids than
solid food
Cont;
• In a latter stage, patients may develop significant weight loss due to
poor caloric intake
• In the acute or chronic phase of obstruction, continuous vomiting may
lead to dehydration and electrolyte abnormalities
• When obstruction persists, patients may develop significant and
progressive gastric dilatation
• The stomach eventually loses its contractility
• Undigested food accumulates and may represent a constant risk for
aspiration pneumonia
Metabolic changes in GOO
• Initial phase or compensated phase
Prolonged vomiting of gastric contents (mainly fluid rich in H and CL)
Water loss- dehydration
H&CL Loss- hypochloraemic alkalosis
For compensation,
Kidneys secrete urine with low CL content& high HCO3 (alkaline urine)
HCO3 excretion- to compensate metabolic alkalisis but at the expense of Na ion
Dehydration&Hyponatraemia
Cont;
• Late phase or decompensate phase
Continue vomiting- more dehydrated & hyponatraemic
RAA system activation
Na is retained by kidneys by the action of aldosterone
For Na reabsorption, 1st K then H excreted
Paradoxically acid urine
More severe alkalosis and hypokalaemia
Cont;
• Alkalosis reduces plasma ionized calcium- feactures similar to
hypocalcaemia develop
• Late tetany
• Chvostek’s sign- twitching of facial muscles on tapping of facial nerve
• Trousseau’s sign- tetanic spasm of hand following blood pressure cuff-induced
arm ischaemia
• Overt tetany
• Neuromuscular irritability manifest as peripheral parasesthesia
• Muscular cramps
• Tetany
Cont;
Clinical Features
History
• H/o long term ulcer symptoms → DU with stenosis
• Symptoms within short duration → malignancy
• More than 90% of patients PUD complaint of abdominal pain which is
typically non radiating burning in quality and located in the
epigastrium
Cont;
• Cardinal symptoms→ Vomiting, Anorexia and Abdominal distention
• Vomiting – typically effortless, projectile, non-billous and present of
partially digested food eaten hours or days previously
• Early stage of obstruction – vomiting is intermittent and usually occur
within one hour of a meal
Cont;
Physical Examination
• General Examination
• Signs of dehydration – skin turgor, dry mouth and sunken eye
• Nutritional anaemia – pallor
• Features of latent tetany – Chvostek’s sign and Trousseau’s sign
Cont;
Abdominal Examination
• Inspection
• Dilated stomach in thin patients – a tympanic mass in the epigastric
area and/or LUQ
• Visible gastric peristalsis (slowly from left to right across abdomen) –
may be elicited by asking the patient to drink a cup of water
Cont;
Palpation
• Dilated stomach
• Succusion splash (Splashing sign) – is done
within 4 hours empty stomach by placing a
stethoscope over the epigastric region and
shaking the patient adequately
Cont;
Auscultopercussion test show dilated stomach
• This test is done by placing a stethoscope over epigastric region
• Skin is scratched from left side downward at several points away from
the epigastrium using finger and these points are joined
• Normally the greater curvature of the stomach lies above the level of
umbilicus while in GOO, it lies below the umbilicus
Investigation
OGD scope
• Required cleansing of stomach
• Direct visualization of lesions
• Can take biopsy for histological assessment
Cont;
Barium meal X-ray
• GOO due to DU with stenosis – 3D
• Dilated stomach
• Delayed gastric emptying
• Deformed duodenal cap
• GOO due to GU – hour-glass stomach and tea-pot deformity
Cont;
Investigation for management
• Blood for CP
• Serum electrolytes
• Total and differential protein
• Urea and Creatinine
Treatment
Fluid and electrolytes correction
• Rehydration by normal saline infusions with potassium supplements
according to electrolytes result
• Successful indicated by
• Increase in urine output
• Fall in blood urea and haematocrit
• Restoration to NL electrolyte concentration
• Blood transfusion may be needed
Cont;
Gastric lavage
• Performed with wide bore tube using saline for irrigation (twice daily)
Aim
• To clear food residue
• To regain stomach tone
• To reduce acid secretion
Cont;
Promote nutrition
• Not allowed patient to eat but fluid and milk drinks should be
encouraged
• If required ,parenteral nutrition
Cont;
Definitive treatment for underlying cause
• Chronic DU- Truncal vagotomy and Gastrojejunostomy
• Other benign causes without acid hypersecretion- gastrojejunostmy
• Hourglass or teapot stenosis d/t GU- partial gastrectomy
• For CA Stomach
• If curative, Radical Gastrectomy
• If palliative, Palliative Resection or Bypass
• Operable Ca head of pancreas- Whipple’s operation
References
• SRB's Manual Of Surgery 7th
Edition
• Baily and Love's Short Practice
of Surgery 28th Edition
Thank You
