GASTRIC OUTLET

OBSTRUCTION

Dr Harshraj Choudhary
Department of Surgery
RNT Medical College, Udaipur
 Introduction
 Gastric outlet obstruction (GOO) is a condition where the
opening between the stomach and small intestine is
blocked either partially or completely.
 It is not a single entity or disease, but rather a clinical and
pathophysiological consequence of any disease process
that produces a mechanical or non-mechanical impediment
to gastric emptying. 
 This portion of the stomach where the blockage is located
is known as the pylorus, hence the alternative term for
gastric outlet obstruction – pyloric obstruction.
Normal movement of food through the
stomach
 Food and fluid enters the stomach from the esophagus through the
top of the stomach known as the cardia. It is then mixed with
stomach acid and digestive enzymes.
 Strong muscular contractions of the stomach churns the food with
these enzymes. This assists with chemical digestion but also helps
break down the food into smaller pieces as part of mechanical
digestion.
 Eventually it is transformed into semi-solid mixture which is then
pumped out of the stomach through the pylorus. Larger solids
remain behind in the stomach until it is broken down further.
 The two common causes of gastric outlet obstruction are
(i) Gastric cancer and
(ii) Pyloric stenosis secondary to peptic ulceration.
 Previously, the latter was more common.
 Now, with the decrease in the incidence of peptic ulceration and
the advent of potent medical treatments, gastric outlet obstruction
should be considered malignant until proven otherwise, at least in
resource-rich countries.
 The term ‘pyloric stenosis’ is normally a misnomer.
 The stenosis is seldom at the pylorus.
 Commonly, when the condition is due to underlying peptic ulcer
disease, the stenosis is found in the first part of the duodenum,
the most common site for a peptic ulcer.
 True pyloric stenosis can occur due to fibrosis around a
pyloric channel ulcer.
 However, in recent years the most common cause of gastric
outlet obstruction has been gastric cancer.
 In this circumstance the metabolic consequences may be
somewhat different from those of benign pyloric stenosis
because of the relative hypochlorhydria found in patients
with gastric cancer.
 EPIDEMIOLOGY
The
 incidence of gastric outlet obstruction (GOO) is not precisely known, though it is likely
lower in recent years due to the decrease in peptic ulcer disease (PUD).
The clinical entities that cause GOO are generally categorized into two well-defined groups—

benign and malignant. Before the identification of Helicobacter pylori (H. pylori) and the
advent of H2-receptor antagonists, when PUD was more prevalent, benign causes of GOO
were more common than malignant causes.
Today, this ratio is reversed, with recent reviews reporting that 50% to 80% of all cases are

attributable to an underlying malignancy. The leading benign cause of GOO remains PUD,
although the incidence is very low, with GOO occurring in only approximately 2% of patients
with PUD.
In contrast, the incidence of GOO complicating primary pancreatic, gastric, or duodenal

malignancy is reported to be as high as 15% to 25%.
Etiology
BENIGN

 Peptic Ulcer disease

 Ingestion of Caustics
Trichobezoars ( Hairballs)
Adult hypertrophic Pyloric stenosis
Pyloric mucosal diaphragm
Pancreatic Pseudocysts

BARIATRIC PROCEDURES
Vertical banded gastroplasty
 Roux-en-Y gastric bypass
Etiology
MALIGNANT

Carcinoma of Stomach
Periampullary carcinomas
Carcinoma Head of pancreas
Ampullary carcinoma
Carcinoma of second part of duodenum
Cholangiocarcinomas
Other causes of gastric outlet obstruction

Adult pyloric stenosis

This is a rare condition and its relationship to the childhood
condition is unclear, although some patients have a long history
of problems with gastric emptying.

Pyloric mucosal diaphragm

The origin of this rare condition is unknown. It usually does not
become apparent until middle life. When found, simple excision
of the mucosal diaphragm is all that is required.
Clinical features

 In benign gastric outlet obstruction, there is usually a long

history of peptic ulcer disease. Nowadays, as most patients
with peptic ulcer symptoms are treated medically, the
condition is becoming much less.

 In this circumstance, the metabolic

consequences may be somewhat different
from those of benign pyloric stenosis because
of the relative hypochlorhydria found in
patients with gastric cancer.
 Clinical Presenation
 Vomiting is the principal symptom with undigested food
particles and nonbilious nature of vomitus usually within 1 to 2
hrs of food intake
 Progressive weight loss and malnutrition
 Earlysatiety, bloating, anorexia, epigastric fullness are other
symptoms
 On examination, patient may be dehydrated and malnourished
with presence of a tympanitic mass in the epigastrium and left
hypochondrium with presence of succession splash.
Vomiting Visible gastric hyperperistalsis
 Metabolic effects
 These are most interesting, as the metabolic consequences of
benign pyloric stenosis are unique.
 The vomiting of hydrochloric acid results in hypochloraemic
alkalosis. Initially the sodium and potassium may be relatively
normal. However, as dehydration progresses, more profound
metabolic abnormalities arise, partly related to renal dysfunction.
 Initially,
the urine has a low chloride and high bicarbonate
content, reflecting the primary metabolic abnormality. This
bicarbonate is excreted along with sodium, and so with time the
patient becomes progressively hyponatraemic and more
profoundly dehydrated.
 Because of the dehydration, a phase of sodium retention
follows and potassium and hydrogen are excreted in
preference. This results in the urine becoming
paradoxically acidic and hypokalaemia ensues.
 Alkalosis leads to a lowering in the circulating ionised
calcium, and tetany can occur.
Metabolic complications

 Loss of acid in gastric vomiting lead to hypochloremic metabolic alkalosis

 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.
 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
 Thus, paradoxical aciduria is a consequence of renal attempt to correct
hypochloremia.
 So final result is hypokalemic, hyponatremic, hypochloremic metabolic
alkalosis with paradoxical aciduria.
INVESTIGATIONS
 CBC
 S/E
 LFT
 Test for H. pylori
 ABG s : Metabolic Alkalosis
 Urine C/E: paradoxical aciduria
Radiology
 Plane X-ray Erect Abdomen
 Large Gastric shadow
 Large amount of Gastric fluid
Barium Meal
6 hour period of fasting is observed prior to
study
 Barium sulphate is ingested by the patient
 X-ray images are taken at 20 to 30 minutes
interval in supine position
Barium Meal
Diagnoses
(1) 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.

(2) Nuclear gastric emptying studies, barium upper GI

studies, Upper GI endoscopy can also be used as indicated.
(3) CECT abdomen can also aid in diagnoses especially when
periampullary or pancreatic pathology is suspected.
Management
 Two Aims:

(1) Correct metabolic abnormality

(2) Deal with mechanical obstruction
Correcting Metabolic Abnormalities
 Pass double large Bore IV line
 Pass wide bore nasogastric tube to empty the stomach
 Sometimes an orogastric tube is required to lavage and
empty the stomach as nasogastric tube may not be
sufficiently large to deal with contents of the stomach
 Intravenous
Normal Saline (0.9% NaCI) with Potassium
Supplementation
 Correct anemia
Management
 Early cases may settle with conservative management
 NPO
 ANTACIDS
 PPI
Surgery for benign GOO
Pyloroplasty with vagotomy
Truncal Vagotomy and Antrectomy and Billroth
Reconstructions
PYLOROPLASTY
 FINEY
 JABOULEYS
 Heineke-Mikulicz
GASTROJEJUNOSTOMY
BALLOON DIALATATION
 ENDOSCOPIC DALATION
 Repeated dilatations needed
 May cause perforation
Endoscopic stenting for
unresectable tumor
Stenting