SUP GIB Flashcards
Stress ulcers
Form of hemorrhagic gastritis that may occur in patients who have had a major stressful event
NSAID ulcers vs stress ulcers
Stress ulcers cause more congestion and bleeding than NSAID-induced ulcers
Will eventually involve multiple sites in the GI tract
Hypothesized pathogenesis
Acid hypersecretion
Reduction in GI mucosal blood flow during acute injury and impaired perfusion of the gut
Reduction in normal protective mechanisms during acute injury
Risk factors (only need 1) for SUP
Mechanical ventilation Coagulopathy (PLT < 50,000, INR > 1.5) Thermal injury Severe head or spinal cord injury GI bleeding or ulceration within past year Multiple trauma Perioperative transplant period Low intragastric pF Surgery > 4 hours Acute lung injury
Risk factors (2+) for SUP
Sepsis syndrome ICE stay > 1 wk Occult bleeding High dose corticosteroids Hepatic failure Acute renal insufficiency Hypotension Anticoagulation
Pharmacologic SUP
Sucralfate
Antacids
H2RAs
PPIs
Sucralfate MOA
Works by coating and protecting the gastric mucosa
Which medications for SUP require a functioning GI tract?
Sucralfate
Antacids
Sucralfate frequency
Must be dosed frequently
What toxicity is possible with sucralfate?
Aluminum
Which SUP can cause tolerance?
H2RAs
What ADR is rare in H2RAs
Thrombocytopenia
Other agents for SUP?
Misoprostol
Enteral feedings
Allopurinol
Dimethyl sulfoxide
GIB locations
Can occur in multiple sites
Definitions of GIBs
Upper (5x more common)
Lower
Occult (unknown to pt)
Obscure (from an unknown site in the GI tract)
Increased risk for patients with GIBs
> 60 years of age
In shock
With poor overall health status
Co-morbid illnesses
Types of GIBs
Variceal
Non-variceal
Causes of non-variceal GIB
Peptic ulcer
Mallory-Weiss tears
Less/frequent rare causes: tumors, Crohn’s disease, arteriovenous malformation
Peptic ulcers caused by
Primarily caused by H pylori Stress ulcers ASA NSAID Radiation Chemo Zollinger-Ellison syndrome Vascular insufficiency
Mallory-Weiss tear
Tear in the mucosal layer at the junction of the esophagus and stomach
GIB s/sx
Hematemesis Melena Hematochezia Anemia Tachycardia Orthostasis Hypotension Fatigue Weakness Ab pain Pallor Dyspnea
The use of what medications would we look for in a pt hx?
Anti-platelet agents NSAIDs Warfarin Directa cting oral anticoagulants Heparin LMWH Thrombolytic agents GPIIb/IIIa receptor antagonists Direct thrombin inhibitors
How does GIB affect bowels?
May be hyperactive in acute GIB - Bowel sounds will be affected
Labs in GIB
CBC Coagulation parameters Fecal occult blood test LFTs BUN
Diagnostic tests for GIB
Endoscopic exams (pre-endoscopic IV PPI is recommended)
- Sclerotherapy
- Thermal coaptive therapy
Basic treatments of GIB
If intravascular volume is low, it should be replaced
Acid suppression
If coagulopathy is present, this must be corrected. Any of the following may need to be done
When is risk of re-bleeding greatest in GIB?
w/in 72 hours of initial presentation
What intragastric pH is necessary to prevent clot dissolution?
> 6
Guidelines recommend which drugs to increase pH in GIB?
PPI
Which PPIs are in IV form?
Nexium
Protonix
When is it okay for oral PPIs after endoscopy in GIB?
If endoscopy only deteched flat-spot or clean-based ulcer (no clot)
Pharmacotherpay follow-up considerations (after endoscopy of GIB)
Test for H pylori (repeat if negative) and treat H pylori infection if present. No need for PPI after eradication
If non-H pylori bleed, continue oral PPI therapy for 6-8 weeks
Stop NSAIDs if possible - if not possible it is recommended to use a cox-2 inhibitor in combination with an oral PPI
If low-dose ASA is required, reinitiate when CV risks outweight GI risks (add a PPI)
Assess for ability to stop anticoagulants. If patients must remain on them, arrange for close follow up and add a PPI
