Patients that don’t respond to PPI trial are warranted a full investigation to identify peptic ulcers, H. pylori and R/O malignancy of the stomach and esophagus, using: CBC and stool occult blood Endoscopy with biopsy (especially in older patients) Urea breath test/serology/stool Ag Medical management is warranted if peptic ulcer disease is the definitive diagnosis Avoid smoking, alcohol, NSAIDs Use of antacids to relieve symptoms PPI for isolated ulcers (no H pylori) H. pylori +ve triple therapy (PPI + amoxicillin + clarithromycin) or quadruple therapy (PPI + tetra + metro + bismuth) Surgical management is only indicated in PUD if “ICHOP”: Intractable to medical Rx Cancer possibility (in gastric ulcers) Hemorrhagic features Outlet obstruction (GOB) Perforated peptic ulcer (usually duodenal) Peptic ulcer disease Acute ulcer disease (usually secondary to gastritis) NSAIDs use (hemorrhagic gastritis) Stress ulcers (in ICU patients, shocked patients) Cushing ulcers (in increased ICP, probably increased vagal tone) Curling ulcers (in burn patients) Chronic ulcer disease (classic peptic ulcer disease) Risk factors: Family history Smoking and alcohol use Age (DU occurs at age 40s-50s; GU later ages) H. pylori infection Chronic NSAIDs use Chronic steroid use Possible causes to consider: Hypercalcemia (hyperparathyroidism) Zollinger-Ellison syndrome (suspected when intractable and on endoscopy many ulcers are seen, even in jejunum; gastrin levels are >1000 pg/mL = pathognomonic)
Obstruction occurs at two points (proximal and distal) Requires emergency surgery Occurs in incarcerated hernias, torsion, adhesions, volvulus Pathophysiology: Obstruction results in proximal air-fluid collection and distal decompression Increased intestinal activity (peristalsis) to overcome the obstruction (contracting against a blocked tube) results in colicky pain (early) Bowel wall edema and increased intraluminal contents and pressure Disruption of venous and then arterial circulation Ischemia (strangulation) and then necrosis occurs Perforation peritonitis, septicemia & shock & death Risk factors: Previous abdominal operations (MC RF) Hernia Inflammatory bowel disease (especially CD stricture SBO) Ingested foreign body Hx of cholecystitis/cholelithiasis (risk to develop gallstone ileus) Presentation: Symptoms: Colicky abdominal pain (diffuse/central) Abdominal distention N&V (proximal obstruction produce more vomiting; +/- bilious & feculent odor) Constipation: does not pass stools but may pass gas Obstipation: does not pass stool or gas (more likely to be complete) Signs: Unstable patient (patient appears unwell, altered mental status, dehydrated, tachycardic +/- fever, BP drop) Abdominal distention, visible peristalsis, previous operation scars Hyperactive bowel sounds on auscultation (high pitched tinkling sounds)
ABC NPO, NGT decompression LGIT decompression by: Rectal tube Colonoscopy Cholinergic drugs (neostigmine) Surgery LOWER GI BLEEDING: Bleeding originating from GI source BEYOND the ligament of Trietz However, be aware that in general, we R/O upper GI sources before lower GI sources Upper GI sources of bleeding usually present with melena or occult blood, however brisk UGI bleeding can present with hematochezia Presentation Hematochezia Bright red blood per rectum Usually indicates lower GI source of bleeding (or brisk UGI source) Melena (not as often) Right sided LGI bleeding may present with darker hematochezia or melena Hemodynamic instability: Anxious Tachycardia Orthostatic hypotension (>20 SBP drop on standing) Hypotension, altered mental status/confused Etiology: Diverticulosis bleeding (MCC ~ 40%) By group: Anatomic Diverticulosis Acute hemorrhoidal bleeding & anal fissures Intussusception (currant-Jelly stool) Meckel’s diverticulum (painless) Vascular Angiodysplasia Ischemic colitis (HF, shock patient, AAA repair) Radiation induced Inflammatory Infectious colitis (e.g. pseudomembranous) IBD (ulcerative colitis) Neoplastic CRC bleeding & polyp Management & investigations: