Stress ulcers commonly occur within 1-2 days of ICU admission and have a high mortality rate of 50-70% in critically ill patients. They involve multiple superficial gastric erosions that are diffuse in nature and do not respond to endoscopic therapy. Stress ulcers are caused by decreased gastric blood flow and mucosal ischemia due to factors like hypovolemia, reduced cardiac output, and inflammatory mediator release in critically ill patients. Prophylaxis and early resuscitation have significantly reduced the occurrence of stress ulcer-related major bleeding in ICU patients.

2.  It occurs in most patients within 1-2 days after ICU
admission.
 50-70% mortality in critically ill pts
 There is clinically sig. decrease in SRMD due to
prophylaxis & early resuscitation

3.  Multiple superficial erosive lesions occuring
early in the course of critial illness, and may
progress to deep ulcers
 Stress ulcers are difuse in nature and do not
respond to endoscopic therapy, heal over
time w/o intervention.

4. Stress ulcers Peptic ulcers
Multiple superficial lesions at the
proximal stomach bulb; involves
superficial capillaries; results from
splanchnic hypoperfusion
Few deep lesions in the
duodenum; typically involves a
single vessel; results from break in
gastric, duodenal, or esophageal
lining from the corrosive action of
pepsin

5. 1. Decreased gastric blood flow and mucosal
ischemia are the primary causes of stress
ulcer–related bleeding.

6.  Hypovolemia
 Reduced cardiac output
 Proinflammatory mediator release
 Increased catecholamine release
 Visceral vasoconstriction

7.  Decreased gastric mucosal bicarbonate
production
 Decreased gastric emptying of irritants and
acidic contents
 Acid back-diffusion
 Reperfusion injury that may occur after
restoration of blood flow after prolonged
periods of hypoperfusion

9.  respiratory failure requiring mechanical ventilation
for ≥48h
OR
 coagulopathy: platelet count <50 000 cells/mm3,
INR> 1.5, or aPTT >2x normal

10.  renal failure
 Age (>50 yrs)
 Male
 Acute respiratory failure
 MI
 AKI
 Neurologic injury
 Sepsis
 Shock
 acute/chronic hepatic failure
 Coagulopathy
 severity of illness, liver dz, & renal replacement
therapy.

11.  Spinal cord/head trauma
 Thermal injury affecting >35% of total BSA
 Hx of GIB w/in the past year
 Postoperative transplantation
 Ulcerogenic medications (NSAIDs, Aspirin, CS

13.  Dose-dependent.
 Not rcd for routine use b/c of frequency of
administration (up to qh) S.E & intx.
 S.E: diarrhea, constipation, electrolyte
abnormalities.

14.  Complexes with albumin and fibrinogen to form a
viscous, adhesive substance that adheres to
ulcers in the presence of a pH less than 4
 less effective than H2RAs.
 Not rcd for routine use b/c of S.E. and intx by
chelation
 S.E: constipation, aluminum toxicity,
hypophosphatemia

15.  MOA:Competitive blockade of histamine subtype 2
receptors on the basolateral membrane of the parietal
cells
 Dose-dependent increase in gastric pH
 Adverse effects such as mental status change,
thrombocytopenia, sinus bradycardia and risk for
nosocomial pneumonia.
 Drug interactions with CYP450 isoenzymes and PH
dependent interaction.
 Dosing: Cimitidine: 300mg IV/PO q6h or continuous
infusion at 37.5-50mg/hr
Ranitidine: 150mg PO q12h, or 50mg IV q8h

16.  MOA: Inhibiting active proton pumps.
 Prodrug
 Dose-dependent increase in gastric pH,
with maximal activity reached 3 days
after initiation.
 Rebound acid hypersecretion may occur
after discontinuation.
 Drug interactions: all are hepatically
metabolized by CYP450 isoenzymes
and PH dependent interaction

17.  S.E: Diarrhea, abdominal pain, constipation,
nausea, Headaches, Rash, Interstitial
nephritis, Hypomagnesemia, Neurologic
effects, Hypophosphatemia and metabolic
alkalosis when administered with sodium
bicarbonate, Vitamin B12 deficiency,
Increased risk of fractures (hip, waist, and
spine) ,CDI, Risk of nosocomial pneumonia

18.  Overt Bleeding + one of the following:
1. Decrease in BP 20 mmHg w/in 24h of the
first GIB episode
2. Decrease in BP 10 mmHg & increase HR 20
BPM on orthostatic change
3. Decrease in Hg 2 g/dl & transfusion of 2
units of blood w/in 24 h if bleeding OR
failure of Hg conc. Increase after transfusion
by at least # units tranfered – 2g/dl