Should We Transfuse Patients with Subarachnoid Hemorrhage?
Abstract & Commentary
By Andrew M. Luks, MD, Pulmonary and Critical Care Medicine, University of Washington, Seattle, is Associate Editor for Critical Care Alert.
Dr. Luks reports no financial relationship to this field of study.
Synopsis: Although anemia was predictive of adverse outcomes in patients with aneurysmal subarachnoid hemorrhage, red blood cell transfusion was also associated with an increased risk of death, severe disability or delayed infarction. These results call into question the practice of liberal transfusion thresholds in patients with spontaneous subarachnoid hemorrhage.
Source: Kramer AH, et al. Crit Care Med. 2008;36: 2070-2075.
Delayed ischemic insults are a major cause of morbidity and mortality in spontaneous subarachnoid hemorrhage (SAH). Recognizing this risk, some clinicians have argued that patients with SAH should be transfused to target hemoglobin levels of 9-10 g/dL in an effort to maintain oxygen delivery. In light of other studies demonstrating adverse outcomes with red blood cell (RBC) transfusion, Kramer and colleagues sought to determine what effect, if any, anemia or transfusion had on patient outcomes in spontaneous SAH.
The authors conducted a single-center retrospective cohort study. Patients who developed spontaneous SAH from a ruptured cerebral aneurysm over a 4-year period were included in the analysis while those patients in whom life-sustaining care was withdrawn within 72 hours of admission were excluded. One of the authors reviewed all of the records to collect information such as nadir hemoglobin concentrations, RBC transfusions, and a large number of other variables. Patients were reportedly managed according to "published guidelines." Anemia was defined as a hemoglobin concentration below 10 g/dL while vasospasm was thought to be present if patients had (1) a change in neurologic status not explained by another etiology; (2) vascular imaging interpreted by a neuroradiologist as demonstrating radiographic vasospasm and; (3) symptoms that were sufficiently severe for physicians to start treatment. The primary outcome was a combined endpoint of death, severe disability or delayed infarction with neurologic outcomes assessed at 6 weeks using the Glasgow Outcome Scale. Secondary outcomes included development of nosocomial infections and ARDS. A variety of statistical analyses were used to make comparisons between transfused and non-transfused patients and between anemic and non-anemic patients.
There were 245 patients included in the statistical analysis. Eighty-five patients (35%) were transfused an average of 2.5 units of blood with mean pre-transfusion hemoglobin concentrations of 9.5 g/dL (range 7-13). Both anemia and transfusion were associated with an increased risk of the combined primary endpoint (odds ratio for anemia: 2.7, 95% CI: 1.5-5; odds ratio for transfusion 4.8, 95% CI: 2.5-9.1). When both variables were included in the logistic regression model, transfusion, but not anemia, was still associated with an increased risk for the combined endpoint. The relationship between anemia and the combined endpoint was stronger among those patients with vasospasm (OR 3.8) whereas for transfusion, the odds ratio for the combined endpoint was higher among those patients who did not have vasospasm (OR 3.5). There was no association between transfusion and the subsequent diagnosis of vasospasm. Transfusion had no effect on the development of ARDS but was predictive of the development of nosocomial infections. The duration of blood storage had no effect on outcomes.
Commentary
This is another study in a growing line of recent studies examining the impact of RBC transfusions on patients with various forms of critical illness. It is noteworthy that although anemia was associated with poor outcomes in patients with spontaneous SAH, transfusions were as well. Given that the relationship between anemia and adverse outcomes was stronger among those patients who were diagnosed with vasospasm while the relationship between transfusion and adverse outcomes was stronger among those patients without vasospasm, the paper suggests that rather than applying a single transfusion strategy to all of our SAH patients, we should possibly be tailoring our transfusion practices based on their clinical course and, in particular, whether or not they are having vasospasm.
In considering the results and their implications, however, several issues must be considered. This was a single center retrospective study and, as a result, may not be as applicable as the prospective randomized trial by Hebert and colleagues1 that established current transfusion practices in critically ill patients. The fact that this is a single center study is particularly important in light of the discipline involved in the study. Although the authors stated that they adhered to "published guidelines" for the management of their patients, there is little in the way of randomized controlled data to guide the care of patients with SAH. In fact, only a single intervention in this patient population, nimodipine prophylaxis for vasospasm, has randomized controlled data to support its use while "Triple-H" therapy (hemodilution, hypertension, hypervolemia), one of the mainstays of vasospasm management, has little, if any, in the way of supporting evidence.2 As a result, there is considerable inter-institution and inter-physician variability in the care of SAH patients and it is possible that similar effects of anemia and transfusion might not be seen in a multi-center setting, particularly if different transfusion practices are used at other institutions. The mean pre-transfusion hematocrit in this study, for example, was 9.5 g/dL, a high threshold that may not be used across all institutions.
Nevertheless, the results of this paper are generally consistent with those of many recent papers looking at the impact of RBC transfusions in critically ill patients. As a result, we need to stop treating SAH like it's the "heart attack of the brain" and transfusing all of these patients as we would someone with acute coronary syndrome. More restrictive practices may be warranted until further studies can be completed on this issue.
References
- Hebert PC, et al. N Engl J Med. 1999; 340: 409-417.
- Treggiari MM, et al. Systematic review of the prevention of delayed ischemic neurologic deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg. 2003; 98: 978-984
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