Its a Gastric Outlet Obstruction topic based on situations in the resource challenged countries

1. 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