(Stroke. 1996;27:421-424.)
© 1996 American Heart Association, Inc.
Articles |
Gastrointestinal Hemorrhage After Acute Stroke
From the University of Edinburgh, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland.
Correspondence to R.J. Davenport, Department of Clinical Neurosciences, University of Edinburgh, Western General Hospital, Crewe Rd, Edinburgh, Scotland EH4 2XU. E-mail rjd@skull.dcn.edinburgh.ec.uk.
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Abstract |
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 Top Abstract IntroductionSubjects and Methods Results Discussion References |
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Background and Purpose Although patients with critical illness or acute head injury are known to be at risk of gastrointestinal hemorrhage, there is little information concerning acute stroke. We sought to record the frequency, possible causes, and course of gastrointestinal hemorrhage in a cohort of hospitalized stroke patients.
Methods During a 36-month period we prospectively identified 613 strokes (excluding subarachnoid hemorrhage). We then retrieved the case notes, and a single observer reviewed all available records (n=607), noting any episodes of gastrointestinal hemorrhage together with details concerning the course, possible precipitating factors, management, and outcome.
Results Eighteen patients (3%) experienced a gastrointestinal hemorrhage, half of which were severe. These patients were older and had suffered more severe strokes than those without any gastrointestinal bleeding. The source was identified in 5 patients; 2 had gastric ulceration, 2 duodenal ulceration, and the remaining one had esophageal/duodenal ulceration. In 17 patients there was a potential risk factor for hemorrhage, although the odds ratios comparing the use of antithrombotic drugs in the hemorrhage and nonhemorrhage groups did not achieve statistical significance. Death during the acute admission period was more common in the 18 hemorrhage patients (odds ratio, 4.6; 95% confidence interval, 1.7 to 13.2; two-tailed P=.002, Fisher's exact test); of the 10 who died, gastrointestinal hemorrhage appeared to have been a contributing factor in 3.
Conclusions Our study provides a reasonably accurate estimate of the frequency of gastrointestinal hemorrhage after acute stroke. The higher frequency found in our study than the previously published data is probably due to study methodology. Older patients with more severe strokes may be at increased risk of this complication, and it may adversely affect outcome.
Key Words: complications • gastrointestinal hemorrhage • stroke outcome
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Introduction |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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Patients admitted to intensive care units are at risk of gastrointestinal hemorrhage, which is usually due to acute hemorrhagic gastritis ("stress" ulceration).1 2 The risk may be even higher in head-injured patients, occurring in up to 75% of patients with severe trauma.3 Therefore, it seems plausible that patients who have suffered an acute stroke may also be at a similarly high risk of gastrointestinal hemorrhage, which may be further exacerbated by the use of antithrombotic drugs. However, there are few published data on this topic; only one4 of the several studies that have described poststroke complications commented on gastrointestinal hemorrhage, and the subject is not included in several recent reviews of stroke complications.5 6 7 8 Wijdicks et al9 published a study based on coded discharge data of 16 612 patients admitted with an acute stroke and found a frequency of only 0.1%. In addition, a randomized trial of prophylactic H2 antagonists in stroke patients with a Glasgow Coma Scale score of 10 or less suggested a frequency of 65%.10 These estimates did not seem to match our own experience, and therefore we aimed to document the frequency, course, management, and predisposing factors of this complication in a hospital-based study.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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We prospectively identified consecutive patients who were either admitted to the medical unit of our hospital with an acute stroke (first ever or recurrent) or suffered a stroke while already an inpatient; all patients were assessed by an experienced stroke physician before entry into a stroke register. We used the World Health Organization definition of stroke11 but excluded subarachnoid hemorrhage. We then attempted to retrieve the case notes of all patients, and a single observer (R.J.D.) reviewed all the available records (medical and nursing notes), recording all episodes of gastrointestinal hemorrhage together with details of their management, possible predisposing factors, and outcome. We defined a gastrointestinal hemorrhage as any recorded episode of hematemesis or melena in the records or autopsy evidence of a recent hemorrhage. We did not include isolated, equivocal recordings such as "vomiting with ?coffee grounds" or "?dark stools" unless there was other substantiating evidence (eg, hypotension or a fall in hemoglobin). We used the presence of hypotension (systolic blood pressure <100 mm Hg) and/or a fall in hemoglobin of more than 2 g/L to define a severe gastrointestinal hemorrhage.
We performed univariate analyses using a number of
different variables to determine which were associated with
gastrointestinal hemorrhage (Figure
); we
dichotomized age into greater or less than the median age of the whole
sample (73 years). We also dichotomized the prestroke Oxford Handicap
Scale grade into independent (0 to 2) and dependent (3 to 5); total
anterior circulation infarcts12 were compared with
non-total anterior circulation infarcts (hemorrhagic strokes
excluded). Since five subjects of the hemorrhage group were
dysphasic, we used the motor and eye-opening components of the
Glasgow Coma Scale rather than a composite score. We recorded
urinary incontinence occurring within 7 days of stroke as an additional
marker of stroke severity.
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Results |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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During a 36-month period we identified 613 strokes occurring in 597 patients; 47 of these occurred in patients already hospitalized for other reasons. Case notes were available for 607 (99%) of these strokes. The mean length of stay was 37 days, allowing 22 459 patient-days of observation in our study. Gastrointestinal hemorrhage complicated 18 (3%; 95% confidence intervals, 2% to 5%) of these 607 strokes; 9 of these hemorrhages were severe, as defined above. Details of these patients are shown in the Table
; their mean age was 78 years (SD, 8.9),
significantly older than the rest of the cohort (mean age, 71 years;
SD, 12.3; two-tailed P=.02, two-sample t
test).
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Seventeen patients presented with hematemesis and/or melena; the exception (patient 13) developed abdominal pain and hemodynamic shock and was thought clinically to have perforated a viscus, but autopsy revealed a gastric ulcer with fresh and altered blood throughout the gastrointestinal tract.
The source of the hemorrhage was identified in only 5 of our
patients (2 gastric and 2 duodenal ulcers, 1 esophageal and duodenal
ulceration). Only 2 patients were investigated during life; in the
others, the attending physicians thought it inappropriate to
investigate further, either because the patient was too ill or because
the hemorrhage was thought insignificant. All but 1 patient
(patient 2) had a potential predisposing or exacerbating factor for
gastrointestinal hemorrhage (Table
), although in 4 (1 after
surgery, 2 with disseminated carcinoma of the prostate, and 1 with
anemia of unknown cause) the association was very uncertain (neither
carcinoma patient had the relevant tests performed to exclude
coagulopathy).
Univariate analyses showed that
gastrointestinal hemorrhage patients were significantly older
and more disabled before their stroke and had more severe strokes
compared with the nonhemorrhage patients (Figure); the use
of antithrombotic drugs was not a significant risk factor.
The prognosis of the patients who suffered a gastrointestinal hemorrhage was poor; 10 of the 18 patients died in the hospital. Compared with the other 589 strokes, the odds of dying in the hospital were 4.6 (95% confidence interval, 1.7 to 13.2; two-tailed P=.002, Fisher's exact test). However, assessing the contribution of the gastrointestinal hemorrhage to these 10 deaths on retrospective case note review was difficult. Undoubtedly, all those who died were in a poor neurological condition before death (7 had suffered a total anterior circulation stroke and 6 had either a Glasgow Coma Scale motor component <6 or eye component <4 on admission). However, in 3 patients (patients 7, 13, and 18) bleeding contributed directly to their death. In the other 7 patients it is unlikely that it influenced the final outcome; 5 of these patients were not expected to survive before the bleeding, and in the remaining 2 (patients 9 and 17) death occurred 28 and 21 days after the hemorrhage, respectively.
Five patients received blood transfusions and another 6 intravenous fluids. Nine patients were started on an H2 antagonist and 1 on omeprazole; only 3 of the 8 surviving patients were discharged on prophylactic medication against further hemorrhage. One patient was discharged on aspirin and another on warfarin after a deep venous thrombosis.
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Discussion |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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The frequency of 3% in our study is higher than that found by Dobkin4 (1% in a sample of 200), who used a methodology similar to ours (although he did not publish his diagnostic criteria). Both these estimates are considerably higher than that found by Wijdicks et al.9 We suspect that differences in study design may account for much of the difference; in their study, Wijdicks et al relied on coded discharge diagnoses to identify their patients and found just 17 episodes in 16 612 patients admitted with stroke during an 18-year period. Although we doubt that the record keeping in our hospital is quite as accurate as that of the Mayo Clinic, it is notable that only 5 of our 18 patients were assigned a correct International Classification of Diseases, 9th Revision discharge code relating to their gastrointestinal hemorrhage. Thus, relying on routine statistics would have led us to underestimate the true frequency by two thirds. In addition, it is unclear how long the patients were under observation; for most of the study period, our hospital provided an integrated package of care from the time of acute admission to discharge (either home or to a long-term care facility) or death, which is reflected in the mean length of stay of 37 days. Studies based in either acute-care units or rehabilitation centers may miss either late or early hemorrhages, respectively. All of the hemorrhages in the Mayo study occurred within 2 weeks of the stroke, whereas in ours 5 occurred later than this. Wijdicks et al acknowledged that they may have missed minor bleeds and concluded that the true frequency of gastrointestinal hemorrhage in stroke remains unknown. We believe that our study provides a more accurate estimate of the frequency of this problem, although the retrospective design does have flaws. We are intrigued by the study of Machfoed et al,10 who reported that cimetidine reduced the frequency of gastrointestinal hemorrhage after severe stroke from 65% to 6%; thus far this has appeared only in abstract form and does not contain sufficient detail to allow further comment. Whether gastrointestinal hemorrhage is a stroke-specific complication or more generally associated with acute brain events (or even more generally associated with elderly patients admitted with other primary pathologies) is interesting to consider; unfortunately, since we did not include a control group, our study cannot provide an answer.
One problem we experienced due to the retrospective design was the identification of bleeding events from the case notes. When a large hemorrhage occurred, this was usually clearly recorded. Otherwise, it was sometimes unclear from the notes whether a hemorrhage had occurred. Patients who vomited or developed diarrhea after their stroke were common; accompanying the entries recording these episodes (usually in the nursing section) were sometimes equivocal comments regarding the vomitus or stool (eg, "?coffee grounds" or "?dark/black motion"), and sometimes normal-appearing vomitus/stool tested positive for blood with bedside strip testing. Should these patients be included as gastrointestinal hemorrhages? We decided not to include such equivocal events (in the absence of any other substantiating evidence), but it is possible that by doing so we have underestimated the true frequency. To overcome this problem, a prospective study, with the use of predefined diagnostic criteria, is required. In addition, one of our patients was not thought to have had a hemorrhage in life, and yet autopsy showed evidence of extensive hemorrhage, which undoubtedly precipitated her death. Thus, it is possible that the low autopsy rate (29% of the 134 patients who died during their acute admission) may have led to a further underestimate of the true frequency of gastrointestinal hemorrhage.
No source of the hemorrhage was identified in most of our
patients, although few were investigated (Table). In four cases
(including both cases of hemorrhagic stroke), hematemesis occurred in
the setting of headache, nausea, and recurrent vomiting at the onset of
neurological symptoms, which suggests that these may have been related
to either gastritis/esophagitis or a Mallory-Weiss tear. As in the
series of Wijdicks et al,9 we noted a high prevalence of
potential risk factors for hemorrhage. However, although
aspirin13 14 and anticoagulation may either
precipitate or
exacerbate bleeding, the confidence intervals of the odds ratios
included unity. Nonsteroidal drugs15 and
steroids16 are associated with gastrointestinal
hemorrhage, but unfortunately we did not record the
use of these drugs in the nonhemorrhage group and
therefore could not calculate odds ratios. The association of gastric
bleeding and a percutaneous endoscopic gastrostomy tube
is very rare but has been noted previously.17 18
Our study suggests that hemorrhage occurs in older stroke patients who have more prestroke disability and in those with more severe strokes (as indicated by stroke subtype,12 Glasgow Coma Scale score, and urinary incontinence within 7 days of stroke onset). Wijdicks et al9 found that hemorrhage was life threatening in only one of their patients compared with our series, in which it seems to have played a significant part in the deaths of at least 3 patients and was associated with hypotension or a significant fall in hemoglobin in an additional 6. This poor outcome is not surprising; older patients, particularly those who have other morbidity, have a higher mortality after gastrointestinal hemorrhage.19 Although we cannot conclude anything concerning the effect of gastrointestinal hemorrhage on the neurological deficit, it seems theoretically plausible that hypotension and/or anemia, particularly in the acute phase after stroke onset, may be detrimental.
The frequency, even at 3%, does not seem high enough to warrant studies of prophylactic treatment for all patients; based on this frequency, we estimate that more than 4000 patients would be needed to satisfactorily demonstrate a relative risk reduction of 50%. However, prophylactic treatment in patients with severe stroke might be an area suitable for further investigation, although it is worth remembering that the evidence to support prophylactic treatment of gastrointestinal hemorrhage in other critically ill patients remains equivocal.20 21
We conclude that our study provides a reasonable estimate of the frequency of gastrointestinal hemorrhage after acute stroke. Although the frequency is low (3%), it does seem that hemorrhage may be clinically significant and lead to death; despite this, it is unlikely that trials of prophylactic treatment for all patients are warranted. Physicians who care for acute stroke patients should be aware of this uncommon but potentially serious complication.
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Acknowledgments |
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This study was supported by the Medical Research Council (UK) (Dr Davenport and the Stroke Register) and the Stroke Association (UK) (Dr Dennis).
Received September 5, 1995; revision received November 16, 1995; accepted November 21, 1995.
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