GASTRIC OUTLET OBSTRUCTION

Dr. Shahzad Alam Shah

Gastric outlet obstruction (GOO, pyloric
obstruction) is not a single entity----


Clinical and pathophysiological consequence
of any disease process that produces a
mechanical impediment to gastric emptying
Causes
Two well-defined groups of causes
Benign & Malignant

In the past-- peptic ulcer disease more
prevalent, benign causes most common

Now-- only 37% have benign disease and
the remaining have obstruction secondary to
malignancy
Diagnostic and treatment dilemma


Exclude functional nonmechanical causes of
obstruction, such as diabetic gastroparesis

Once mechanical--- differentiate between
benign and malignant ( definitive Tt varies)

Diagnosis and treatment Urgent, because delay
further compromise pts. nutritional status
Delay also further compromise edematous
tissue and complicate surgical intervention

Frequency

The incidence less than 5% in pts. with PUD--
leading benign cause


Peripancreatic malignancy, the most common
malignant etiology--- 15-20%.

Etiology

Major benign causes of gastric outlet
obstruction (GOO) are---

PUD
gastric polyps
ingestion of caustics
pyloric stenosis
congenital duodenal webs
gallstone obstruction (Bouveret syndrome)
pancreatic pseudocysts
and bezoars

Etiology(Contd)

PUD --- 5% of all patients with GOO

Ulcers within the pyloric channel & D-1
responsible for outlet obstruction

Obstruction -- Acute -- secondary to acute
inflammation and edema , Chronic--
secondary to scarring and fibrosis

Helicobacter pylori

Etiology(Contd)

Pediatric age group--- Pyloric stenosis
Pyloric stenosis occurs in 1 per 750 births
Boys Girls
More common in first-born children

Pyloric stenosis ---- gradual hypertrophy of the
circular smooth muscle of the pylorus
Etiology(Contd)

Pancreatic cancer is the most common
malignancy causing GOO
Outlet obstruction may occur in 10-20%
Other tumors include---
Ampullary cancer
Duodenal cancer
Cholangiocarcinomas
Gastric cancer
Metastases to the gastric outlet by other
primary tumors
Pathophysiology

Intrinsic or extrinsic obstruction of the pyloric channel or duodenum

Intermittent symptoms that progress until obstruction is complete.
Vomiting is the cardinal symptom. Initially, better tolerance to liquids
than solid food

In a later stage, significant weight loss due to poor caloric intake.
Malnutrition is a late sign, -- very profound in patients with concomitant
malignancy

Continuous vomiting may lead to dehydration and electrolyte
abnormalities

When obstruction persists, may develop significant and progressive
gastric dilatation

The stomach eventually loses its contractility. Undigested food
accumulates ------------- constant risk for aspiration pneumonia

Clinical features

Nausea and vomiting are the cardinal symptoms
Vomiting -- Nonbilious, and it characteristically
contains undigested food particles
Early stages --- vomiting intermittent and
usually occurs within 1 hour of a meal
Very often it is possible to recognize foodstuff
taken several days previously
Pt. loses weight, appears unwell & dehydrated


Clinical features(Contd)
GOO from a duodenal ulcer or incomplete obstruction
typically present with symptoms of-----------

Gastric retention, including early satiety, bloating or
epigastric fullness, indigestion, anorexia, nausea,
vomiting, epigastric pain, and weight loss
Frequently malnourished and dehydrated and have a
metabolic insufficiency
Weight loss , most significant with malignant disease

Abdominal pain is not frequent and usually relates to
the underlying cause, eg, PUD, pancreatic cancer

Physical examination
Chronic dehydration and Malnutrition
On examination :
Distended stomach and a succussion splash
may be audible on shaking the patients
abdomen

A dilated stomach may be appreciated as a
tympanitic mass in the epigastric area and/or
left upper quadrant
Metabolic effects
Dehydration and electrolyte abnormalities-- Increase in
BUN and creatinine are late features of dehydration
Prolonged vomiting causes loss of hydrochloric acid &
produces an increase of bicarbonate in the plasma to
compensate for the lost chloride-------hypokalemic
hypochloremic metabolic alkalosis
Alkalosis shifts the intracellular potassium to the
extracellular compartment, and the serum potassium is
increased factitiously
With continued vomiting, the renal excretion of
potassium increases in order to preserve sodium
The adrenocortical response to hypovolemia intensifies
the exchange of potassium for sodium at the distal tubule,
with subsequent aggravation of the hypokalemia

Paradoxically acidic urine
Initially, the urine has a low chloride and high bicarbonate
content, reecting 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.
Alkalosis leads to a lowering of the circulating ionised calcium,
and tetany can occur.
Management

Involves
Correcting the metabolic abnormality &
Dealing with the mechanical problem
Rehydrated with i/v isotonic saline with
potassium supplementation. Replacing the
sodium chloride and water allows the kidney
to correct the acidbase abnormality
Following rehydration it may become
obvious that the patient is also anaemic, the
hemoglobin being spuriously high on
presentation
Management(contd)

The stomach should be emptied using a
Wide-bore gastric tube. Pass an nasogastric
tube and lavage the stomach until it is
completely emptied
Then endoscopy and contrast radiology
Biopsy of the area around the pylorus is
essential to exclude malignancy
The patient should also have an anti-
secretory agent, initially given intravenously
to ensure absorption




Management(contd)

Early cases -- settle with conservative treatment,
(Oedema around the ulcer diminishes as the
ulcer is healed)

Severe cases treated surgically, usually with a
gastroenterostomy rather than a pyloroplasty

Endoscopic treatment with balloon dilatation --
useful in early cases
(Dilating the duodenal stenosis may result in
perforation, and the dilatation may have to be
performed several times and may not be
successful in the long term)
Indications(Surgery)

GOO due to benign ulcer disease may be treated
medically if results of imaging studies or
endoscopy determine - acute inflammation and
edema are the principle causes (as opposed to
scarring and fibrosis, which may be fixed)

If medical therapy -- fails, then surgical
Typically, if resolution or improvement is not
seen within 48-72 hours, surgical intervention is
necessary
The choice of surgical procedure depends upon
the patient's particular circumstances

In cases of malignant obstruction, weigh the
extent of surgical intervention for the relief of
GOO against the malignancy's type and extent,
as well as the patient's anticipated long-term
prognosis
As a guiding principle, undertake major tumor
resections in the absence of metastatic
disease(in fit pts)
In patients with largely metastatic disease,
determine the degree of surgical intervention
for palliation in light of the patient's realistic
prognosis and personal wishes
Summary
Gastric outlet obstruction is most commonly
associated with longstanding peptic ulcer disease and
gastric cancer
The metabolic abnormality of hypochloraemic
alkalosis is usually only seen with peptic ulcer disease
and should be treated with isotonic saline with
potassium supplementation
Endoscopic biopsy is essential to determine whether
the cause of the problem is malignancy
Endoscopic dilatation of the gastric outlet may be
effective in the less severe cases of benign stenosis
Operation is normally required, with a drainage
procedure being performed for benign disease and
appropriate resectional surgery if malignant