Nancy A. Melville

May 04, 2017

LOS ANGELES — An early elevated white blood cell (WBC) count represents a strong predictor of delayed cerebral ischemia after subarachnoid hemorrhage (SAH) in patients with good clinical grade, new research suggests.

"The utility of the admission WBC as a measure of systemic inflammation following SAH is simple, cost-effective and most importantly can provide us with an indication of likelihood of developing delayed cerebral ischemia," first author, Fawaz Al-Mufti, MD, told Medscape Medical News.

"Good-grade patients without elevated WBC may be candidates to be safely downgraded from the [intensive care unit], leading to cost savings for both patient families and hospitals," said Dr Al-Mufti, from the Department of Neurosurgery at Rutgers New Jersey Medical School, Newark.

The findings were presented here at the American Association of Neurological Surgeons (AANS) 2017 Annual Meeting.

Despite advances in the treatment of SAH, delayed cerebral ischemia remains a leading cause of morbidity and mortality, with events typically starting within several days of the initial bleed.

With a multitude of possible factors in the cause of delayed cerebral ischemia, Dr Al-Mufti and colleagues focused on a potential role of immune dysregulation as a key cause.

To further investigate the role, the authors evaluated data on 849 patients with aneurysmal SAH who were part of a larger observational cohort study and who had white blood cell differentials obtained within 72 hours of the bleed onset.

After adjustment for known predictors of delayed cerebral ischemia, including patients' clinical grade, a thick SAH on admission computed tomography (CT), smoking status, and clipping aneurysm repair, the results showed that a WBC count of 12.1 × 109/L or higher was a strong predictor of delayed cerebral ischemia (odds ratio [OR], 1.2; 95% confidence interval [CI], 1.1 - 1.3;  P < .001).

A neutrophil-lymphocyte ratio of 5.9 or higher was also significantly associated with the development of delayed cerebral ischemia (OR, 1.7; 95% CI, 1.1 - 2.2; P = .008).

WBC counts were elevated in 49% of patients considered of good clinical grade, defined as a Hunt and Hess classification of 1 to 3, and those patients had an increased hazard for delayed cerebral ischemia equivalent to that in patients with poor clinical grade (hazard ratio, 2.1; 95% CI, 1.3 - 3.2; P < .001).

An elevated WBC count in patients of good clinical grade was shown in additional receiver-operating characteristic analysis to represent an even a stronger predictor of delayed cerebral ischemia (area under the curve [AUC], 0.63) than the standard predictor of a modified Fisher scale (AUC, 0.57).

Patients with good clinical grade and WBC counts of 12.1 or lower were meanwhile significantly less likely to experience delayed cerebral ischemia (P < .001).

A neutrophil-lymphocyte ratio of 5.9 or higher was also a stronger predictor than modified Fisher scale, with an AUC of 0.59, positive predictive value (PPV) of 26%, and negative predictive value (NPV) of 86%.

A combination of WBC count and the modified Fisher score produced an even stronger predictor of delayed cerebral ischemia, Dr Al-Mufti added.

"We found that when you include the WBC count and modified Fisher scale, you get an overall fair AUC of 0.73 and PPV of 34% and an excellent NPV of 92%."

Predictors of elevated WBC counts in good-grade patients included younger age, white ethnicity, a medical history of diabetes, ictal loss of consciousness, physiologic derangement, aneurysm location, and the presence of more SAH blood, he said.

Dr Al-Mufti noted that the mechanisms behind the association between WBC count and delayed cerebral ischemia after SAH are likely complex.

"Our initial hypothesis was that an elevated WBC count following SAH reflected a heightened inflammatory reaction and immune response that may predict susceptibility to delayed cerebral ischemia and could be important in understanding the clinical course in patient following SAH," he said.

Inflammation could, for instance, lead to a hypercoagulable state, leading to microembolism in the brain in the setting of cerebral vasospasm, with inflammation further leading to the susceptibility to neuronal injury.

He noted, however, that much more needs to be understood to validate the role of WBC.

"Further research is needed to prospectively validate the effect of admission WBC and to determine whether this finding represents a modifiable factor or if treatment may mitigate its impact."

Dr Al-Mufti has disclosed no relevant financial relationships.

American Association of Neurological Surgeons (AANS) 2017 Annual Meeting. Abstract 604. Presented April 24, 2017.


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