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Duodenal Ulcer
- characteristics: mostly occurs in 40-65 yo, M:F = 2:1, more than twice as common as gastric ulcers, bleed 4x as often as gastric ulcers, 25% of total UGI bleeds
- etiology
- most (95%) due to H. Pylori
- increased gastric acid production
- environmental factors – smoking, NSAIDs
- risk factors: male, smoking, aspirin/NSAID use, uremia, Zollinger-Ellison syndrome, H. pylori infection, trauma, burn injury
- sx: epigastric pain (burning or aching, several hrs after meal, initially relieved by food, milk, or antacids), back pain, N/V, anorexia, decreased appetite
- signs: tenderness in epigastric area (possibly), guaiac-positive stool, melena, hematochezia, hematemesis
- ddx: acute abdomen, pancreatitis, cholecystitis, all causes of UGI bleeding, Zollinger-Ellison syndrome, gastritis, MI, gastric ulcer
- diagnose with H&P, EGD, UGI series (if not actively bleeding), urea breath test, H. pylori serology
a. with EGD, visible vessel in ulcer crater a/w 90% rebleed rate
- location
- majority within 2 cm of pylorus in duodenal bulb
- posterior – more likely to bleed b/c erodes into gastroduodenal artery
- anterior – most likely to perforate (see free air under diaphragm on upright AXR)
- medical tx
- Antacids (Mg, Al, Ca): control gastric pH, promote healing
- H2 receptor blockers: usually heal ulcers in 4-6 wks
- Sucralfate: coats ulcer
- Proton pump inhibitors (omeprazole): decrease acid production; used for refractory ulcers and ulcers a/w Zollinger-Ellison syndrome
- Prostaglandins: provide mucosal protection
- Bismuth
- Antibiotics: triple therapy for H. pylori (see above)
- surgical tx
- indications: I HOP
I = Intractability
H = Hemorrhage (massive or relentless)
Note: exsanguination is the most common cause of death from a duodenal ulcer
O = Obstruction (gastric outlet obstruction)
P = Perforation
- goal: decrease gastric acid secretion and fix IHOP
- options for Intractability
- highly selective vagotomy (preserves pyloric branches, operation of choice b/c only 0.5% mortality, but increased recurrence, 10-25%)
- vagotomy and pyloroplasty (0.5-1% mortality, 10-12% recurrence)
- vagotomy and antrectomy Billroth I or II (1-2% mortality, 1-2% recurrence) (see Surg Recall p.235 for Billroth I, II explanations)
- for Hemorrhage, open duodenum through pylorus, oversew bleeding vessel, perform vagotomy and pyloroplasty
- options for Obstruction
- truncal vagotomy, antrectomy, and gastroduodenostomy (Billroth I) or gastrojejunostomy (Billroth II)
- truncal vagotomy and drainage procedure (gastrojejunostomy)
- options for Perforation
- Graham patch for poor candidates, shock, or prolonged perforation (Graham patch is a piece of omentum incorporated into the suture closure of a perforation)
- truncal vagotomy and pyloroplasty, incorporating ulcer
- Graham patch and highly selective vagotomy
- truncal vagotomy and antrectomy
- complications
- early
- hemorrhage (may need to reoperate)
- gastric retention from vagotomy
- duodenal stump leakage with Bilroth II (must usually reoperate)
- late
1. dumping: ealy dumping: uncontrolled emptying of hypertonic fluid from intravascular space to intraluminal space, leading to intravascular volume depletion and diarrhea; late dumping: rapid absorption of glucose due to improper gastric emptying, leads to large insulin increase – over-correction of blood glucose leads to transient hypoglycemia approx. 3 hrs after meal
2. diarrhea (tx with Lomotil, Kaopectate, Imodium)
3. reflux gastritis (convert Billroth I/II to gastrojejunostomy)
- gallstones
- weight loss
- iron/vit B-12 deficiency due to decreased intrinsic factor secretion (tx with supplementation)
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