Mock33CC Gastric outlet obstruction
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Stem: 67-year-old woman presents to her GP with 10 days history of vomiting with gastric content. This can occur any time and has no associated factors. At the GP surgery she collapsed but does not lose consciousness. The ambulance takes her to ED, on arrival she has pulse of 105, BP 105/55 and epigastric fullness was noted.
Why hypokalaemia hypochloremic metabolic alkalosis?
Persistent vomiting (chloride, hydrogen)
Bicarbonate used in production of gastric acid secret in blood because of acid is loss more. More bicarbonate in the blood when ability of the gut and kidney to Excrete or saturated
Increase creatinine, because hypovolemia decreases renal perfusionWhy hypokalaemia??
Loss vomiting
K+/Na+ exchangeIn addition to the fluid resuscitation what bedside procedure can help in the bowel problem?
NGT
CatheterAs surgical registrar, who will be involved ?!
Surgical consultant
HDU / level 2 nursing staff or Anaesthesia team (line placement).When patient will be fit for the surgery?
Corrected electrolyte and metabolic disturbance.
Optimal iv fluid resuscitation??
I will give this patient sodium chloride, plus potassium supplement to:
-replace sodium and chloride and potassium
-correct of the metabolic component better than Hartman (more chloride)Clinical picture of hyponatremia?
Confusion, cerebral oedema
Seizures
Cardiac arrhythmia disturbancesWhy aciduria?
Dehydration will lead to increase aldosterone which happens DCT and collecting duct. Here Na+ reabsorbed in exchange K and hydrogen ion.
Classification of hyponatremia & give example for each?
According to Serum osmolarity can be divided to isotonic, hypotonic and hypertonic hyponatremia.
Then hypotonic hyponatremia can be divided according to volume status to:
Hypovolemic hyponatremia e.g. diarrhoea, vomiting and diuretics
Euvolemic hyponatremia e.g. SIADH, hypothyroidism
Hypervolemic hyponatremia, e.g. heart failure
Pseudohyponatremia: Multiple myelomaComplications of hyponatremia?
Brain: cerebral oedema, seizures and decrease consciousness level, confusion
Heart: MI and heart failure
Respiratory: SOB, Chest pain
Liver: hepatic encephalopathy
Kidney: renal failureCauses of gastric outlet obstruction?
Benign -> pyloric stenosis secondary to chronic peptic ulceration.
Malignant -> (gastric or pancreatic) carcinoma.Is NaHCO3 excreted as a whole ion?
Yes
What is Chloride shift?
Is the shift of the chloride ion to the intra-cellular compartment of RBC in exchange of bicarbonate ion excretion.
What is the single bedside test you should do?
ABG
What is the clinical picture of GOO
Dehydration.
Non bilious vomiting
Left hypochondrial fullness
Visible peristalsis -
- What are the common causes of gastric outlet obstruction in adults?
The causes can be divided into benign and malignant.
Benign
Peptic ulcer disease causing pyloric stenosis
Chronic pancreatitis
Caustic ingestion
Post-surgical strictures
Crohn’s disease
Malignant
Distal gastric cancer (most common modern cause)
Pancreatic head cancer
Duodenal carcinoma
Periampullary tumours
Historically peptic ulcer disease was the commonest cause, but malignancy is now more common.- Why does gastric outlet obstruction cause vomiting of undigested food?
The obstruction occurs at the pylorus or proximal duodenum, preventing gastric emptying.
Food therefore remains in the stomach for prolonged periods and is vomited before reaching the small intestine, so it appears undigested.- What electrolyte and acid–base abnormalities are classically seen?
The classical abnormality is:
Hypochloraemic
Hypokalaemic
Metabolic alkalosis
Often associated with hyponatraemia and volume depletion.- Why does vomiting lead to metabolic alkalosis?
Gastric secretions contain hydrochloric acid (HCl).
Vomiting causes loss of:
Hydrogen ions
Chloride ions
Loss of hydrogen ions leads to metabolic alkalosis, and loss of chloride contributes to hypochloraemia, which also impairs renal bicarbonate excretion and worsens the alkalosis.- Why does hypokalaemia occur in gastric outlet obstruction?
Hypokalaemia occurs due to:
Renal potassium loss from activation of the renin–angiotensin–aldosterone system due to dehydration.
Hydrogen–potassium exchange in the kidney during metabolic alkalosis, where potassium is excreted to retain hydrogen ions.- What clinical signs might you find on examination?
Possible signs include:
Epigastric distension
Succussion splash (if stomach contains retained fluid)
Visible gastric peristalsis
Signs of dehydration (tachycardia, hypotension)
Possible weight loss if chronic- What investigations would you perform to confirm the diagnosis?
Investigations include:
Blood tests: FBC, U&E, LFTs, ABG
Nasogastric aspiration (large residual volume)
Upper GI endoscopy (OGD) – confirms obstruction and allows biopsy
CT abdomen – helps identify malignancy or extrinsic compression
OGD is the key diagnostic test.- How would you manage this patient initially?
Initial management is resuscitation and decompression:
Nil by mouth
Nasogastric tube for gastric decompression
IV fluids to correct dehydration
Correct electrolyte abnormalities
IV proton pump inhibitor
Arrange urgent endoscopy
Definitive treatment depends on the cause (e.g., endoscopic dilation, surgery, or oncological treatment).
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