Global Cerebral Edema After Subarachnoid Hemorrhage
To the Editor:
We have read with great interest the article by Claassen et al on cerebral edema after subarachnoid hemorrhage (SAH).1 Their results are in agreement with those we presented in another recent article.2 When analyzing the factors associated with bad prognosis at hospital admission in 294 patients suffering SAH admitted to our center during a 10-year interval, global cerebral hypodensity was present in 7% of the patients, a figure similar to that presented by the authors. Global brain hypodensity stood as an independent factor for bad prognosis in both univariate and multivariate logistic regression analyses. In our series, as in this recent article, global brain hypodensity in the admission CT was clearly related to mortality, as more than 90% of patients with this factor died, sooner than patients without edema (median 2 versus 10, 2 versus 8 in the Claassen et al series) and more often as a direct result of the hemorrhage (84% in our series).
The analysis of which factors are related to global brain edema is a unique feature of the study by Claassen et al. We have performed the same analysis in our own data, as presented in theTable. The level of consciousness at admission was the main variable related to the presence of global brain hypodensity in our series, and loss of consciousness at stroke was also an associated factor in the univariate analysis. We agree with the mechanisms the authors propose as responsible for the presence of global brain hypodensity. Ictal circulatory arrest and insufficient cerebral perfusion caused by severe intracranial hypertension leads to diffuse ischemic encephalopathy after suffering severe SAH. Several studies using acute MR diffusion-weighted and positron-emission tomographic techniques3,4⇓ have shown widespread ischemic areas in patients suffering poor-grade SAH, supporting that a widespread vascular dysfunction after severe SAH could exist and most probably be responsible for the poor clinical condition of the patients. However, we still do not know whether the presence of the hypodensity on CT is a consequence of this dysfunction or a treatable cause.
The genesis of delayed edema is also considered by the authors, and interestingly it seems that its presence could be partly due to the initial damage to the cerebral circulation caused by the bleeding and to the use of vasopressors. “Triple-H” therapy has not yet gained widespread acceptance, and recently its results have been questioned.5,6⇓ Thus it would be desirable to know which patients could be in danger of developing such a complication, and most probably this will be the subject of further investigation.
Finally, one of the main drawbacks of using brain edema as a prognostic factor is the possible lack of interobserver reliability and/or CT definition when assessing this characteristic. The authors brilliantly solve this problem by accurately defining global and focal edema and achieving good interobserver reliability indexes.
- ↵Claassen J, Carhuapoma JR, Kreiter KT, Du EY, Connolly ES, Mayer SA. Global cerebral edema after subarachnoid hemorrhage: frequency, predictors, and impact on outcome. Stroke. 2002; 33: 1225–1232.
- ↵Lagares A, Gómez PA, Lobato RD, Alén JF, Alday R, Campollo J. Prognostic factors on hospital admission after spontaneous subarachnoid hemorrhage. Acta Neurochir (Wien). 2001; 143: 665–672.
- ↵Lennihan L, Mayer SA, Fink ME, Beckford A, Paik MC, Zhang H, Wu Y, Klebanoff LM, Raps EC, Solomon RA. Effect of hypervolemic therapy on cerebral blood flow after subarachnoid hemorrhage. Stroke. 2000; 31: 383–391.
We thank Dr. Lagares et al for their interest in our study1 and appreciate their confirmatory findings regarding predictors of global edema after subarachnoid hemorrhage (SAH). We believe that this phenomenon has not received enough interest in the past. Data they have presented in their earlier article2 and additional data presented in their reanalysis of their original cohort confirm our findings in terms of the frequency of admission global edema, the earlier timing of death in these patients, and the overall negative impact on outcome.
In addition, their analysis of predictors of admission global edema corroborates the strong association of this entity with admission clinical and radiographic findings. Again, they confirm the key observation that loss of consciousness at onset, which presumably reflects intracranial circulatory arrest, is strongly related to the development of global edema. However, their overall frequency of loss of consciousness was higher than in our study (68% versus 37%). As in our study, none of the admission CT findings remained independent predictors in their multivariate analysis.
We agree that future studies will have to investigate the genesis of global edema and determine whether this is an unpreventable occurrence in a severely inured brain, or if treatment strategies can be developed to prevent its development. MR and CT perfusion imaging may more accurately demonstrate the development of global edema and determine the role of cerebral blood flow abnormalities, microdialysis may help to understand its pathophysiology on a cellular level, and animal studies might be helpful in developing treatment strategies. As it has become clear that most of the burden of morbidity and mortality after SAH is attributable to the direct effects of bleeding,3 it is our hope that early ICU-based resuscitation strategies may allow us to eventually improve the outlook for these extremely poor-grade patients.
- ↵Claassen J, Carhuapoma JR, Kreiter KT, Du EY, Connolly ES, Mayer SA. Global cerebral edema in patients with subarachnoid hemorrhage: frequency, predictors, and impact on outcome. Stroke. 2002; 33: 1225–1232.
- ↵Lagares A, Gómez PA, Lobato RD, Alén JF, Alday R, Campollo J. Prognostic factors on hospital admission after spontaneous subarachnoid haemorrhage. Acta Neurochir (Wien). 2001; 143: 665–672.
- ↵Broderick JP, Brott TG, Duldner JE, Tomsick T, Leach A. Initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage. Stroke. 1994; 25: 1342–1347.