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GASTRIC OUTLET
OBSTRUCTION
DEFINITION
 Gastric outlet obstruction (GOO) represents a clinical
and pathophysiological consequence of any disease
process which produces 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 BUT IN RESOURCE CHALLENGED COUNTRIES WHERE IT
MAY STILL BE THE COMMONEST CAUSE
 Now-- only 37% have benign disease and the remaining have
obstruction secondary to malignancy
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)
 Pancreatic cancer is the most common malignancy causing GOO
 Outlet obstruction may occur in 10-20%
 Ampullary cancer
 Duodenal cancer
 Cholangiocarcinomas
 Gastric cancer
 Metastases to the gastric outlet by other primary tumors
Pathogenesis
 Intrinsic or extrinsic obstruction of the pyloric channel
or duodenum
 Depends upon the underlying etiology
Obstruction of the stomach
Hypertrophy of the stomach
Dilatation
Gastritis & depressed acid secretion
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, 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.
 Alkalosis leads to a lowering of the circulating ionised
calcium, and tetany can occur.
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 recognise 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
Examination
 Chronically ill looking
 Wasted
 Dehydrated
 may be pale due either to a bleeding ulcer, malignancy
 Shock
 Epigastric / Rt hypochondrial tenderness
 Distended abdomen
 Visible gastric peristalsis
 Succussion splash
PRINCIPLES OF MANAGEMENT .
Guiding Principles lies in the
recognition of GOO as an
emergency, as such, GOAL of
treatment include:
-1)Resuscitation/stabilization.;
-2)Relieve obstruction;
-3)Patient selection/categorization;
- patient related factors
-4)Offer definitive curative care;
- Lesion related factors
-5)Prevent recurrence/Follow up care.
Management
Involves
 Correcting the metabolic abnormality &
 Dealing with the mechanical problem
Rehydrated with i/v isotonic saline with potassium supplementation/
Ringer’s . Replacing the sodium chloride and water allows the kidney
to correct the acid–base abnormality
investigations
1) Stabilise patient
 FBC (anaemia)
 SEUCR (hypochloraemia,
hypokalaemia,hyponatraemia,elevated Hco3)
 BLOOD GASES(metabolic alkalosis)
 URINALYSIS (paradoxical aciduria)
investigation
2)To confirm diagnosis
 Plain x-ray of abdomen:shows large gastric shadow and a large
amount of gastric fluid.
 Gastric aspiration:a wide bore stomach tube is placed early in the
morning and the stomach is aspirated of resting juice.if >400ml of
juice is obtained a presumptive diagnosis of GOO can be made.
investigation
 Esophagogastroduodenoscopy + biopsy(histology and bacterioloical
investigation).
Aim is to visualise the stomach mucosa and any ulcer.
 Barium meal:
-markely dilated stomach with a lot of residue
-presence of an ulcer crater
-trifoil deformity of the duodenal cap.
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
THE CHALLENGES HERE
 The commonest cause is chronic PUD
 Diagnostic challenge in terms of a CT scan, though
can still be done
 Laboratory challenge in determining the metabolic
anomalies
 Best to use Ringer’s for resuscitation as potassium is not
easily available
SUMMARY
 In poor resource countries, the best diagnostic
modality still remains to be clinical ( non- bilious
vomitus within an hour of taking a meal, gastric
peristalsis and succution splash)
 the availability of PPIs and eradication therapy for
H.pyroli has made the incidence of malignancy to be
on the rise as the cause of GOO

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Gastric Outlet Obstruction

  • 2. DEFINITION  Gastric outlet obstruction (GOO) represents a clinical and pathophysiological consequence of any disease process which produces mechanical impediment to gastric emptying
  • 3. Causes Two well-defined groups of causes— Benign & Malignant  In the past-- peptic ulcer disease more prevalent, benign causes most common BUT IN RESOURCE CHALLENGED COUNTRIES WHERE IT MAY STILL BE THE COMMONEST CAUSE  Now-- only 37% have benign disease and the remaining have obstruction secondary to malignancy
  • 4. 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
  • 5. Etiology(Contd)  Pancreatic cancer is the most common malignancy causing GOO  Outlet obstruction may occur in 10-20%  Ampullary cancer  Duodenal cancer  Cholangiocarcinomas  Gastric cancer  Metastases to the gastric outlet by other primary tumors
  • 6. Pathogenesis  Intrinsic or extrinsic obstruction of the pyloric channel or duodenum  Depends upon the underlying etiology
  • 7. Obstruction of the stomach Hypertrophy of the stomach Dilatation Gastritis & depressed acid secretion
  • 8. 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
  • 9. Paradoxically acidic urine  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.  Alkalosis leads to a lowering of the circulating ionised calcium, and tetany can occur.
  • 10. 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 recognise foodstuff taken several days previously  Pt. loses weight, appears unwell & dehydrated
  • 11. 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
  • 12. Examination  Chronically ill looking  Wasted  Dehydrated  may be pale due either to a bleeding ulcer, malignancy  Shock  Epigastric / Rt hypochondrial tenderness  Distended abdomen  Visible gastric peristalsis  Succussion splash
  • 13. PRINCIPLES OF MANAGEMENT . Guiding Principles lies in the recognition of GOO as an emergency, as such, GOAL of treatment include: -1)Resuscitation/stabilization.; -2)Relieve obstruction; -3)Patient selection/categorization; - patient related factors -4)Offer definitive curative care; - Lesion related factors -5)Prevent recurrence/Follow up care.
  • 14. Management Involves  Correcting the metabolic abnormality &  Dealing with the mechanical problem Rehydrated with i/v isotonic saline with potassium supplementation/ Ringer’s . Replacing the sodium chloride and water allows the kidney to correct the acid–base abnormality
  • 15. investigations 1) Stabilise patient  FBC (anaemia)  SEUCR (hypochloraemia, hypokalaemia,hyponatraemia,elevated Hco3)  BLOOD GASES(metabolic alkalosis)  URINALYSIS (paradoxical aciduria)
  • 16. investigation 2)To confirm diagnosis  Plain x-ray of abdomen:shows large gastric shadow and a large amount of gastric fluid.  Gastric aspiration:a wide bore stomach tube is placed early in the morning and the stomach is aspirated of resting juice.if >400ml of juice is obtained a presumptive diagnosis of GOO can be made.
  • 17. investigation  Esophagogastroduodenoscopy + biopsy(histology and bacterioloical investigation). Aim is to visualise the stomach mucosa and any ulcer.  Barium meal: -markely dilated stomach with a lot of residue -presence of an ulcer crater -trifoil deformity of the duodenal cap.
  • 18. 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
  • 19.  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
  • 20. THE CHALLENGES HERE  The commonest cause is chronic PUD  Diagnostic challenge in terms of a CT scan, though can still be done  Laboratory challenge in determining the metabolic anomalies  Best to use Ringer’s for resuscitation as potassium is not easily available
  • 21. SUMMARY  In poor resource countries, the best diagnostic modality still remains to be clinical ( non- bilious vomitus within an hour of taking a meal, gastric peristalsis and succution splash)  the availability of PPIs and eradication therapy for H.pyroli has made the incidence of malignancy to be on the rise as the cause of GOO