6. HISTORY OF PRESENTING COMPLAINT
Chronically unwell patient
Presented with post-prandial vomiting for a month.
He would vomit undigested food about 2 to 4 hours
after a meal
The vomiting was projectile, non bilious and non
blood stained
Amounted to 1 cupful
It was associated with early satiety and loss off
appetite
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7. HPC CONT...
He reported episodes of passing melena stool but
no diarrhoea and on presentation he had not
been passing stool for the past 6 days
All this was on a background of generalised body
weakness and significant loss of weight( 59kg to
52 kg)
Of note is that the patient had a 20 pack year
history of smoking cigarettes and a 25 year
history of drinking alcohol (8u/day)
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8. HPC CONT...
He did not know his blood group
No family history of malignancy
No history of peptic ulcer disease or chronic use
of NSAIDs
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9. SYSTEMS REVIEW
General: no night sweats. Loss of weight
CVS : palpitations, no oedema, shortness of breath or
dyspnoea
Respiratory: no cough, chest pain, haemoptysis,
GUS: No hematuria, frequency, urgency, dysuria.
MSS: no muscle or joint pain
CNS: no loss of consciousness, headaches, dizziness
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10. PAST MEDICAL AND SURGICAL HISTORY
Index admission was at Mvurwi hospital February 2018 for
generalised body weakness and headache which were
managed and he was transfused 2 units of blood
3months ago he presented to the physicians at PGH with
the same symptoms
Transferred to us from the physicians
No history of other chronic illness
No history of any surgeries
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11. PAST DRUG HISTORY
No history of chronic NSAID use
No known drug allergies
No history of consumption of caustic chemicals
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12. FAMILY HISTORY
No family history of malignancy
No family history of other chronic illnesses
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13. SOCIAL HISTORY
25 year history of drinking alcohol
20 pack year history of smoking cigarettes
Works as a soldier
Married
Modern methods of sanitation
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14. SUMMARY
59 years old male patient who presented
generalised body weakness, profuse postprandial
non bilious vomiting and weight loss. He has no
history of peptic ulcer disease and no personal of
family history of malignancy.
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15. EXAMINATION
Ill looking and wasted with zygomatic
prominence
Palmar pallor
No jaundice, cyanosis or oedema
No generalised lymphadenopathy
Negative trossure sign and no Sr Mary Joseph
nodes
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16. ABDOMEN
I : scaphoid, symmetrical, no masses, no vissible
peristalsis, umbilicus inverted
P: soft non tender, no palpable masses , no guarding
P: flank dullness
A: secussion splash negative, bowel sounds present
DRE: rectum empty, no bloomer’s shelves
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17. For this patient an endoscopic biopsy was done
which showed gastric carcinoma – linitis plastica
Diagnosis was GOO secondary to gastric
malignancy
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18. AETIOLOGY OF GOO
Causes of gastric outlet obstruction may be divided
into Benign or malignant causes.
The aetiology has shifted from mostly benign causes
to mostly malignant causes.
This is due to better medical management of peptic
ulcer disease(PUD)
And the use of H. pylori erradication therapy.
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20. MALIGNANT CAUSES
Pancreatic Cancer (commonest – 10 – 20%)
Duodenal cancer
Peri-ampulary cancer
Cholangiocarcinoma
Gastric cancer
Metastasis to the gastric outlet
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21. PATHOPHYSIOLOGY
There is obstruction of the pyloric channel or of the
duodenum
This may be intrinsic or extrinsic
As a result, post prandial vomiting is the cardinal
feature
- vomiting is non bilious, projectile with
identifiable undigested food.
Initially , liquids are better tolerated than solids
Patients then get significant weight loss due to poor
caloric intake
Malnutrion is a late feature and is more pronounced in
patients with concomittant malignancy
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22. PATHOPHYSIOLOGY CONT...
The profound continuous vomiting then leads to
dehydration and eletrolyte imbalances
When the obstruction persists, patients develop
significant gastric dilatation
- loss of tone of gastric masculature
- gross dilatation
- loss of peristalsis
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23. METABOLIC EFFECTS
Classically, GOO causes a – hypokalemic,
hypochloraemic metabolic alkalosis with
paradoxical aciduria and hypocalcaemia
Prolonged vomiting causes loss of hydrochloric acid
and create a hypochloremic metabolic alkalosis
Dehydration activates the RAAS and this leads to
more Na retention with increases K and H excretion
in the distal tubule – hypokalemic alkalosis
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24. METABOLIC EFFECTS CONT...
Paradoxical aciduria:
-Initially urine has low Cl and high bicarbonate content (reflecting the
primary metabolic abnnormality)
- the bicarbonate is excreted with Sodium and with time the patient
becomes progressively hyponatremic and more dehydrated
-dehydration leads to sodium retention and K and H are excreted
intead
-this leads to acidic urine
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25. CLINICAL PRESENTATION
Nausea and vomiting are the cardinal features
Vomiting is non bilious projectile post-prandial
and contains undigested food materials
In the early stages vomiting may be intermittent
occurring within the first hour of feeding.
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26. PRESENTATION CONT...
If the obstruction is incomplete, the patient gets
retentive symptoms:
-early satiety
-bloating
-epigastric fullness
-indigestion
Malnutrition
Loss of weight
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27. CLINICAL PRESANTATION
On examination
Stomach felt as a dilated tympanitic mass in the epigastric
area
Visible gastric peristalsis
- ‘the stomach that you see’
- ‘the stomach that you feel’
a wave of peristalsis that runs from the left hypochondrium
across the umbilicus to end in the right hypochondrium.
If absent , give patient 500 – 1000 ml of water to drink
Secussion splush – ‘the stomach that u hear’
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29. IMAGING
Upper gastrointestinal endoscopy
-the scope will fail pass down to enter the
duodenum
-a biopsy may be taken during the procedure
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31. INVESTIGATIONS
Barium Meal Xray
-hugely distended stomach
-no or little barium in the esophagus
-mosaic appearance( ba + food)
-delayed evacuation of Ba into duodenum( repeat)
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