ESOPHAGEAL OBSTRUCTION - rEMERGs

More documents

Recommendations

Info

- occurs in 10% of pts w/ GERD - 10% of pts w/ barrett’s esoph have coexistent adenoCa at time of dx - 40Xs risk of Ca than general population - should be followed w/ endoscopy and bx Differential dx ‣ Cardiac ischemia is the main ddx ‣ Note that GERD pain can radiate similar to ischemia ‣ Radiation to abdomen is 3Xs more commonn in GERD than ischemia ‣ Exacerbation of symptoms after meals (fullness sensation) is more suggestive of GERD ‣ Worse with swallowing suggests GERD ‣ Relief by antacids does NOT r/o cardiac Treatment ‣ Does NOT target H. pylori (not related to GERD) ‣ PHASE I - lifestyle, dietary, elevate bed, avoid factors which dec LES tone, wt lo loss, stop smoking, review drugs, avoid night time eating, dietary review, frequent small meals, symptomatic antacids ‣ ‣ ‣ PHASE II - H2 antagonist ‣ cimetidine (tagamet) 300mg bid ‣ ranitidine (zantac) 150mg bid ‣ famotidine (pepcid)40mg od ‣ nizantidine (axid) 150mg bid - prokinetics ‣ PHASE III - PPIs ‣ ‣ ‣ PHASE IV - sugery (fundal plication) cisapride (prepulsid) 20mg bid - qid (inc LES tone, and inc gastric emptying) omeprazole (losec) 20mg od lanoprazole (prevasid) 30mg od pantoprazole (pantoloc) 40mg od
ABDO PAIN: GASTRIC OR DUODENAL ORIGIN CLINICAL HIGHLIGHTS ETIOLOGY ‣ Peptic Ulcer Disease ‣ Non - ulcer Dyspepsia ‣ Gastritis ‣ Superior Mesenteric Artery (SMA) syndrome ‣ Gastric Volvulus HISTORY ‣ Location ‣ ‣ ‣ Radiation ‣ ‣ ‣ Character ‣ ‣ ‣ ‣ Timing ‣ ‣ ‣ Other ‣ ‣ ‣ ‣ Gastric tends to be epigastrium and slightly left Duodenal tends to be epigastrium and slightly right Back: think perforated duodenal ulcer Shoulder: think perforation of ulcer with subdiaphragmatic air Constant, gnawing: think GU, DU (rarely a colicky pain) Hot, burning, bloating: think gastritis Cramping: think SMA syndrome Gastritis: onset of pain w/i 1hr of eating, food increases pain GU/DU: food relieves pain most commonly (more reliable with DU than GU) DU may waken patient at 0200: think DU b/c gastric secretion increases then (ulcer pain is rarely present on wakening) SMA: precipitated by food Alleviators: antacids decrease 90% of PUD pain and 75% of gastritis pain Onset: very sudden onset think gastric volvulus or perforation PHYSICAL ‣ Peritonitis: perforation or late volvulus with strangulation ‣ Decreased bowel sounds: same ‣ OB+ve stool: bleeding PUD ‣ Virchow’s node: think Ca INVESTIGATIONS ‣ Blood work depends on presentation ‣ AXR: look for free air with perforation or large, distended stomach with volvulus ‣ ECG mandatory in adults MANAGEMENT ‣ NG tube for perforation or suspected volvulus (can’t pass tube) ‣ Emergent OR for perforation or volvulus ‣ Further management depends on working dx
Page 1 and 2: ESOPHAGEAL OBSTRUCTION ANATOMY ‣
Page 3 and 4: ESOPHAGEAL PERFORATION INTRODUCTION
Page 5 and 6: DYSPHAGIA DEFINITIONS ‣ Dysphagia
Page 7 and 8: INVESTIGATIONS ‣ Neck Xrays: look
Page 9 and 10: ‣ Resp Complications: recurrent c
Page 11: GASTROESOPHAGEAL REFLUX DISEASE Int
Page 15 and 16: ‣ ‣ May present w/ Complication
Page 17 and 18: NSAID INDUCED ULCERS EPIDEMIOLOGY
Page 19 and 20: MEDICATION OPTIONS ‣ Gastric Acid
Page 21 and 22: ‣ urease splits urea and produces

ESOPHAGEAL OBSTRUCTION - rEMERGs

Create successful ePaper yourself

Delete template?

Save as template?