Philip Chang, MD
This article by Anderson et al investigates the role of supine bedrest positioning after acute stroke and weighed it against the risk of aspiration pneumonia. In this trial, 11,093 patients were randomized to supine or head-up (defined as at least 30 degrees head of bed elevation) initiated after hospital admission and maintained for 24 hours. The primary outcome was mRS scores at 90 days. The results of the article showed that people who were supine were less likely to maintain a supine position for 24 hours (87% vs. 95%, p<0.001), and there was no difference in mRS scores at 90 days. In addition, there were no significant differences in serious adverse events between the two groups, including the rates of aspiration pneumonia. The authors of the trial suggest that any modification of cerebral blood flow that may have occurred as a result of head positioning initiated within 24 hours was insufficient to reduce neurologic deficit associated with acute stroke.
However, to take away that head positioning is unrelated to risk of neurologic worsening due to decreased cerebral perfusion or aspiration pneumonia for all stroke patients would be cavalier. It is important to underline that for the sake of pragmatic trial design, any type of stroke was admitted into the trial, regardless of mechanism, presence of vascular stenosis, or even hemorrhagic stroke, which makes the results difficult to interpret. For example, hemorrhagic stroke historically leaned toward acute blood pressure control as an attempt to reduce hematoma volume in the hyperacute phase, while ischemic stroke typically focused on permissive hypertension to aid cerebral perfusion. While the study cited the risk of cerebral edema as a reason to include hemorrhagic patients, the range of NIHSS in patients was only 2 to 9, and failed to include severe stroke (NIHSS>21), where the risk of cerebral edema is the greatest. I am also unable to find any data about the prevalence of cerebral edema in the paper or supplementary appendices, and having competing stroke mechanisms can mask any effect size that may have been shown.
In the setting of ischemic stroke, if there is non-salvageable penumbra (i.e. the infarction has completed all ischemic damage possible in that vessel territory), then change in cerebral perfusion is less likely to worsen outcome. This is likely the case in lacunar strokes, which consisted of about 30% of the study population. With the exception of capsular warning syndrome, the vast majority of lacunar strokes likely will not fluctuate with head positioning because the infarction is already completed. Unfortunately, there is no perfusion data for these patients. In my opinion, this perfusion data is most important in the setting of a severe large-vessel stenosis where there is a small core infarction but a large penumbra, such as in the case of severe symptomatic intracranial atherosclerotic disease or severe symptomatic carotid stenosis. This would likely be the patient population benefiting most from head positioning, but, unfortunately, the study did not define which of the strokes were from severe flow-dependent large-vessel stenoses vs. atheroembolic phenomena from unstable large vessel plaque.
In addition, I believe that aspiration pneumonia risk from stroke primarily comes from presence of dysphagia or bulbar weakness. There is no reason to suspect an increased risk of aspiration pneumonia if the patient has a perfectly normal swallow study (for example, a patient with NIHSS=2 from hemianposia). There is no data available on the presence or absence of dysphagia in these patients, and having a large amount of patients without dysphagia (which is possible given low NIHSS scores) would eliminate any effect size that would have been seen by head positioning.
In conclusion, this article suggests that head positioning in acute stroke is unlikely to change patient outcome at 90 days with both risk for neurologic worsening and risk for aspiration pneumonia. I believe from this study that it may be reasonable to allow patients who have a clinically mild ischemic stroke (NIHSS<6), no flow-dependent large-vessel stenosis, and no evidence of penumbra on perfusion imaging to elevate the head of their bed. I also believe that it is reasonable for patients without dysphagia to be supine. However, I worry that patients with the highest risk of poor outcome with elevated head positioning (flow-dependent large-vessel stenosis, or large perfusion deficits) were inadequately represented in this study to generate an effect size. In the future, it would be most interesting to see a study comparing clinical outcomes of head positioning in acute ischemic stroke patients with clinically documented dysphagia and a known perfusion deficit on imaging or a symptomatic large-vessel stenosis.