| |
Introduction
The
development of “stress” ulceration in the upper gastrointestinal (GI)
tract has been part of critical care folklore since the beginning. In 1842
Curling described a series of cases of severe duodenal ulceration
associated with burns; in 1832 Cushing reported ulcer disease associated
with surgery and trauma. In the early years of intensive care, a strong
association between severity of illness and the incidence of GI bleeds was
established. Patients who had major bleeds had a high mortality rate, and,
consequently, prophylaxis against this complication has become a central
issue in ICU care.
What are the major risk
factors?
• The major risk factors are respiratory failure, coagulopathy, sepsis,
hypotension and hepatic and renal failure.
This has been extensively studied: based on the two studies by Deborah
Cooke’s group (1;2), we know that patients with respiratory failure and
with coagulopathy have significantly higher incidences of bleeding than
other patients. The other major risk factors were sepsis, liver failure,
hypotension and renal failure.
Overall, we know that there is a good relationship between severity of
illness (as determined by, for example, Apache II scores) and incidence of
ulceration. Moreover, the longer a patient is in ICU, the more likely they
are to have a GI bleed (3). Patients who are likely to have a number of
these risk factors – burns patients for example (ventilated, hypotensive,
coagulopathic), are more likely to have ulceration and bleeding.
What is the incidence of
stress ulceration?
• The incidence of stress ulceration is diminishing, probably
reflecting better care before and during intensive care admission.
In the 1970s and 80s, meta analyses have put the incidence of overt
bleeding to be approximately 15% (4). The prevalence appears to be
diminishing. Work by Cooke and colleagues ascribed the risk of overt
bleeding to be 4.4% and clinically significant bleeding to be 1.5% (2) The
incidence of clinically significant bleeding appears to be dependent on
severity of illness and the type of patient population studied. For
example, in Perioperative cardiac surgery patients the risk is
approximately 0.4% (5). In stroke patients (who were not mechanically
ventilated) the risk is 0.1% (6). There is a strong relationship between
duration of mechanical ventilation, duration of intensive care stay, and
incidence of ulceration: patients without coagulopathy and mechanical
ventilation had an incidence of bleeding of 0.1% in the earlier Cooke
study (2). Again, duration of care and mechanical ventilation represent
markers of severity of illness rather than direct causes of ulceration.
Suggest a therapeutic
strategy?
• Patients who do not have one of the six major risk factors do not
require treatment.
Patients in shock, sepsis, respiratory, hepatic or renal failure, or who
have a coagulopathy, who are admitted to intensive care, should all be
given stress ulcer prophylaxis. The agent of choice currently is probably
ranitidine, based on best current evidence (although sucralfate remains a
useful alternative). Patients involved in trauma probably also require
prophylaxis, due to their propensity to develop the above problems. There
is no evidence that prophylaxis of other patients, particularly chronic
(non pulmonary) medical and perioperative surgical patients warrant the
expense of prophylaxis.
References
(1) Cook D, Guyatt G, Marshall J, Leasa D, Fuller H, Hall R et al. A
comparison of sucralfate and ranitidine for the prevention of upper
gastrointestinal bleeding in patients requiring mechanical ventilation.
Canadian Critical Care Trials Group. N Engl J Med 1998; 338(12):791-797.
(2) Cook DJ, Fuller HD, Guyatt GH, Marshall JC, Leasa D, Hall R et al.
Risk factors for gastrointestinal bleeding in critically ill patients.
Canadian Critical Care Trials Group. N Engl J Med 1994; 330(6):377-381.
(3) Schuster DP, Rowley H, Feinstein S, McGue MK, Zuckerman GR.
Prospective evaluation of the risk of upper gastrointestinal bleeding
after admission to a medical intensive care unit. Am J Med 1984;
76(4):623-630.
(4) Shuman RB, Schuster DP, Zuckerman GR. Prophylactic therapy for stress
ulcer bleeding: a reappraisal. Ann Intern Med 1987; 106(4):562-567.
(5) Rosen HR, Vlahakes GJ, Rattner DW. Fulminant peptic ulcer disease in
cardiac surgical patients: pathogenesis, prevention, and management. Crit
Care Med 1992; 20(3):354-359.
(6) Wijdicks EF, Fulgham JR, Batts KP. Gastrointestinal bleeding in
stroke. Stroke 1994; 25(11):2146-2148.
Copyright
Patrick Neligan 2001 |
|
|