Supportive and Preventive Medicine
Stress Ulcers
Peptic Ulcers
Several 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
Decreased gastric blood flow and mucosal ischemia are the primary causes of stress ulcerβrelated
bleeding.
Hypovolemia
Reduced cardiac output
Proinflammatory mediator release
| d. | Increased catecholamine release |
|---|
Visceral vasoconstriction
Additional factors leading to stress ulcerβrelated bleeding:
Decreased gastric mucosal bicarbonate production
Decreased gastric emptying of irritants and acidic contents
Acid back-diffusion
| d. | Reperfusion injury that may occur after restoration of blood flow after prolonged periods of |
|---|
hypoperfusion
Studies evaluating risk factors for stress-related bleeding in the presence and absence of SUP are
summarized in Table 3.
Study
Design and Population
Independent Risk Factors
for Bleeding
Notes
N Engl J Med
1994;330:377-81
| β’ | Multicenter, prospective cohort |
|---|
study of 2252 ICU patients
| β’ | Prophylaxis discouraged, |
|---|
except for head injury, burns >
30% of total body surface area,
organ transplantation, evidence
of peptic ulcer disease, or
upper GI bleeding within
previous 6 wk
| β’ | Prophylaxis administered for |
|---|
674 patients (29.9%); agents
included H2RAs, antacids,
sucralfate, prostaglandin
analogues, and omeprazole
| β’ | Mechanical ventilation β₯ |
|---|
48 hr
| β’ | Coagulopathy, defined as |
|---|
Plt < 50,000 cells/mm3,
INR > 1.5, or activated
partial thromboplastin
time > 2 times control
| β’ | Patients with β₯ 2 risk |
|---|
factors had a 3.7%
incidence of bleeding vs.
0.1% if risk factors were
absent
| β’ | Most were cardiothoracic |
|---|
patients; extrapolations
to other ICU settings
potentially inaccurate