Peptic Ulcer Disease and Gastritis

Risk Factors/Etiology
  • H. pylori (most common cause of ulceration)
  • NSAIDs, aspirin common cause of bleeding ulcers and gastritis
  • Alcohol
  • Bile reflux
  • Pancreatic enzyme reflux
  • Gastrinoma (Zollinger-Ellison syndrome)
  • Severe stress (e.g., trauma, burns)
Clinical Presentation and Diagnoses
  • Gastritis and PUD usually are indistinguishable in the ED without endoscopy.
  • Typically epigastric/left upper quadrant burning pain that may radiate to the back after meals.
  • May be relieved by food, antacids (duodenal), or vomiting (gastric).
  • A type and cross match should be sent if the patient is actively bleeding.
  • Helicobacter testing is useful in the primary care setting to guide treatment.
Treatment
  • Iced saline lavage should never be performed. This is a dangerous action. It had been thought that cooling would cause vasoconstriction and accelerate cessation of bleeding, but this is now known to cause arrhythmias without decreasing bleeding.
  • Nasogastric tube. While evacuation of blood from the gut may be one benefit from nasogastric lavage, this procedure can cause great discomfort. It may also be nondiagnostic in a large number of cases, abdominal pain and ultimately the patient will need endoscopy. Therefore early consultation with the gastroenterologist is key.
  • Etiology of gastrointestinal bleeds on endoscopy in those with history of varices found the majority of patients with bleeding were bleeding from acute gastric duodenitis followed by gastric ulcer then duodenal ulcer, varices, Mallory Weiss, esophagitis, fistula.
H2 Blockers and Proton Pump Inhibitors
  • Proton pump inhibitors and H2 blockers are not effective in the acute phase of bleeding. However proton pump inhibitors may help decrease rebleeding after endoscopy.
Vasoconstrictors
  • Vasopressin not too beneficial and risk of hypertension, stroke, coronary ischemia
  • Dose-related decrease in coronary flow and cardiac output
  • Octreotide has a similar mechanism as somatostatin but is more potent and longer acting decreasing splanchnic blood flow and inhibiting gastric acid secretion
  • Patients required less blood transfusion, fewer required surgical and endoscopic intervention after a 100 mcg bolus followed by 25 mcg/h when compared to H2 blockers
  • Given to patients with hematemisis and/or tarry stool and evidence of bleeding peptic ulcer on early endoscopy—subset to which it is applicable
Outpatient Management of UGI

Low risk criteria that have been identified that may warrant outpatient management:

  • No high risk endoscopic feature/varices/portal hypertenisve gastropathy
  • No debilitation
  • No orthostatic vital sign change
  • No liver disease or concomitant disease
  • No anticoagulation or coagulopathy
  • No fresh hematemesis
  • No severe anemia
  • Adequate home support
High Risk Criteria
  • BLEED criteria good screening tool to decide which groups are likely to develop related in-hospital complication. Bleeding, Low systolic blood pressure, Elevated prothrombin time, Erratic mental status, Disease comorbid.
    • 33% of patients with BLEED criteria had complications.
    • Patients with an upper gastrointestinal bleed with signs of hypoperfusion such as syncope, confusion, dizziness or hypotension should have myocardial ischemia excluded.
  • Upper GI bleed
    • Peptic ulcer disease:
      • Risk groups include alcohol use, cigarette use, medications such as NSAID use.
    • Variceal bleeds:
      • Risk groups include those with liver failure and portal hypertension.
      • Variceal bleeds are frightening but remember that most UGI bleeds in patients with varices are from sources other than the varices.
  • If do have variceal bleed, drug therapy to decrease splanchnic flow is first line therapy (vasopressin and octreotide):
    • Vasopressin decreases cardiac output, increases systolic hypertension, arrhythmias and bradycardia. inhibits fibrinolysis and may therefore interfere with hemostasis.
      • Requires a continuous infusion due to short half life (20 min)
      • Somatostatin is more effective in many regards—localized to splanchnic vasculature and produces fewer effects but no difference in all cause hospital mortality
        • When compared, long acting vasopressin and somatostatin (octreotide) equivalent
        • Given the longer half life of octreotide and fewer adverse risks then may be better
        • In last abstract initial control of bleeding achieved in 90% of patients with sclerotherapy and 84% octreotide group.
       
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