Educative approach to a patient with gatrict outlet obstrution.

1. GASTRIC OUTLET
OBSTRUCTION
DZVUKE TREVOR T
MBChB V – UNIVERSITY OF ZIMBABWE
10/17/2019
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2. OBJECTIVES
 Case
 Definition
 Aetiology
 Pathophysiology
 Clinical presentation
 Metabolic derangements
 Investigations
 Management
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3. DEFINITION
 Gastric outlet obstruction is a spectrum of
diseases that produces mechanical impedance to
gastric emptying.
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4. CASE PRESANTATION
Name: CN
Age: 59
Address: stoneridge
Occupation: soldier
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5. PRESENTING COMPLAINT
 Generalised body weakness X 3months
 Post prandial vomiting X 1 month
 Loss of appetite X 1 month
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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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19. BENIGN CAUSES
 Peptic ulcer disease (5% of goo pts)
 Pyloric stenosis
 Inflammatory diseases
- pancreatitis
- crohn’s disease
- cholecystitis
 Caustic ingestion
 Strictures
 Tumors
- lipomas
- adenomas
 Post suregical obstruction
 Pancreatic pseudocysts
 bezoars
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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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28. INVESTIGATIONS
 Imaging
 Blood work
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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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30. INVESTIGATIONS
 Plain abdominal xray
-Distended stomach
-paucity of bowel gas elsewhere
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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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32. BARIUM MEAL
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33. BARIUM MEAL
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34. INVESTIGATIONS
 CXR – exclude mets, aspiration
 USS – exclude ascites
 CT scan Chest , Abdomen and Pelvis – r/o mets
and to stage
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35. INVESTIGATIONS CONT..
 Blood work
 FBC – anemia, reduced Hb and MCV
 U&E – hypokalemia, hypochloremia,
 ABG – metabolic alkalosis, elavated bicarbonate
 LFT – Elavated liver enzymes show metastasis
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36. MANAGEMENT
 Aims are:
-correcting hydration and metabolic abnormality
-dealing with obstruction
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37. INITIAL WORKUP
 Admit
 Insert wide bore i.v cannulae to obtain blood for
(u&e, fbc, crossmatch)
 Wide bore NG tube for stomach decompression
 Rehydrate with
-Normal saline + KCl supplement (IDEAL)
-Ringer’s lactate
 Urinary catheter for output
 Chats to monitor fluid input and output
 Monitor nutrition
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