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home - Stomach - Peptic Ulcer Disease - Postgastrectomy Syndrome Written by Dr Sebastian Zeki
Knowledge

Knows the range of organic and non-organic causes of dyspepsia. Be
aware of current BSG and NICE guidelines for selecting patients for
investigation. Know the significance of alarm symptoms
Understands the relevance of Helicobacter pylori infection and how it
can be detected and treated.
Recognise the adverse effect of nonsteroidal anti-inflammatory drugs
Understands the physiology of gastric acid secretion, mucosal
protection and gastroduodenal motility and know how drugs can
modify these
Knows the complications of ulcer disease, the principles of surgery
that may be required and be aware of post-operative sequelae

Skills
Makes a thorough clinical assessment, perform appropriate
investigations and be familiar with how medical treatments are used.
Show awareness of how to recognise and manage complications

Behaviours
Can explain the steps taken towards making a diagnosis and
planning treatment clearly and comprehensibly

Also....

Knowledge
Knows the causes of upper gastrointestinal bleeding and its
presentation
Understands the circulatory disturbance associated with blood loss
and the pathophysiology underlying the clinical manifestations of
hypovolaemic shock
Knows the principles of assessing hypovolaemia and of restoring the
circulation. Be able to identify and correct coagulopathy
Knows the principles of using the various risk stratification tools SCE 1
Knows how endoscopic techniques are used to control bleeding CbD, DOPS, SCE 1
Understands how oesophageal and gastric varices develop and the
endoscopic and pharmacological methods that are used to control
blood loss

Skills
Can make an accurate clinical assessment, and stratify the risk. Know
the principles of fluid resuscitation and arrange endoscopy
Is aware of methods to secure haemostasis, recognise signs of rebleeding and liaise with other disciplines (such as interventional
radiology or surgery

Behaviours
Assesses and treats patients who have bleeding with appropriate
degree of urgency.

Also...
Knowledge


Understands why part or all of the patient’s stomach is removed and
the altered post-surgical anatomy

Understands the problems of a gastro-enterostomy and a Roux-en-y
anastomosis

Has awareness of dumping syndromes
Knows the various surgical operations performed for obesity (bariatric
surgery) and their complications

Skills
Can give nutritional advice and choose the appropriate method by
which an enteral feeding tube is inserted into the small bowel

Can initiate the use of pancreatic enzyme therapy
Has ability to recognise and treat early and late dumping syndrome
Behaviours
Able to help the patient carers friends and family understand how
the patient can be encouraged to gain weight

Works closely with dieticians and surgical colleagues

Postgastrectomy Syndrome

Postgastrectomy Syndromes100% note a change in their digestive habits postop.20 % significantly affected immediately post-op. 5 % develop lifelong symptoms 1 % are significantly debilitated by these syndromes.Gastric cancer risk — Post gastric resection for benign gastric or duodenal ulcer disease may be at ~5% risk of gastric cancer 15-20 years post-op. No need for surveillance but if done should be 15-20 years post-op with multiple biopsies from the anastomosis and gastric remnant and low threshold to evaluate UGI sx. Postvagotomy diarrhoea In 30 % of patients after truncal vagotomy.Mechanism: Rapid passage of unconjugated bile salts from the denervated biliary tree into the colon, where they stimulate secretion.Treatment: Most cases are self limiting Early Dumping Occurs in 20 % of patients after gastrectomy or vagotomy and drainage.Presentation is with postprandial GI discomfort, which may include N+V+D and cramps, with vasomotor symptoms eg. diaphoresis, palpitations, and flushing.Mechanism involves a rapid emptying of hyperosmolar chyme (particularly carbohy-drates) into small bowel.Leads to net fluid retention due to the osmotic gradient + releases one or more vasoactive hormones, eg. serotonin and VIP Late dumpingClin presentation is the same as early dumping but happens hours after eating. Secondary to hypoglyce-mia from a postprandial insulin peak. Dietary changes (frequent small meals that are high in protein and fat and low in carbohydrates for early dumping; increased carbohydrate consump-tion for late dumping).If intractable (rare)-(Conversion of a vagotomy and pyloroplasty to an antrectomy with Roux-en-Y reconstruction) Chyme H2O INSULIN Alkaline reflux gastritis Occurs in 2% post-opClin Presentation involves persistent burning epigastric pain and chronic nausea that is aggravated by meals.Diagnosis is usually diagnosis of exclusion - OGD may show gastritis/ technetium biliary scan can demonstrate increased reflux of bile into the stomach.There are no effective treaments. Early satietyIt is caused by postsurgical atony, gastric stasis as a result of denervation, or from the "small gastric remnant syndrome" related to resection.Clin Presentations involves epigastric fullness with meals, often followed by emesis.Atony can be identified with a solid food emptying test and may respond to prokinetic agents such as metoclopra-mide and erythromycin. If these fail, completion gastrectomy may be required, although there is some anecdotal evidence that gastric pacing may prove useful.The "small gastric remnant syndrome"- small and frequent meals Afferent and efferent loop syndromes Post Billroth II reconstruction or gastroenterostomy.It is due to mechanical obstruction of the limbs by kinking, anastomotic narrowing, or adhesions.Clin Presentation involves postprandial epigastric pain and nonbilious vomiting relieved by projectile bilious vomiting.The detection of distended afferent loop on CT is diagnostic.Treatments include conversion to a Roux-en-Y anastomosis. Weight Loss and Dietary Resriction (mainly to reduce symptoms of eg early satiety)Malabsorption- accelerated gastric emptying/ reduced gastric seiving (Particles >1mm go through)/ decreased pancreatic functionBacterial overgrowthIron/( 50%)/ B12(20%)/Folate( 40%)Metabolic bone disease Written by Dr Sebastian Zeki Mechanism: Treatment: Diagnosis and Miscellaneous

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