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Instrumental findings compatible with more or less severe degrees of vasospasm were present in almost all our patients, but we considered the vasospasm as clinically relevant only in the presence of unequivocal neurological worsening and/or clear CT findings. Although this could lead to underestimation, the incidence of vasospasm in our series was not negligible, above all if we take into account that those patients who died early probably did not have time to develop it. In any case, the vasospasm did not significantly affect the results. Modern effective therapeutic tools undoubtedly played a role, but many of our patients were already so compromised by the primary damage that little remained to be added by the vasospasm in terms of both mortality and morbidity. Similar deductions could be drawn for the ventricular infections, too: CSF infection occurred in one-third of our patients if we consider the overall series, but in one-half of cases, if we exclude the patients who died early. This relatively high rate probably related to the comatose and very delicate state of these patients, who generally required prolonged external drainage in the contaminated environment of the neurosurgical intensive care unit. Indeed, it is well known that the range of infections may be quite different in different series ranging from 0% to 45% of cases.29 It would depend on the variety of populations evaluated, the use of antibiotic prophylaxis, the technique of catheter placement, the methods of CSF sampling, and the definition of infection adopted (for instance, we considered CSF as infected when either pleocytosis or abnormal CSF protein or AZD7762 levels were evident, even though the CSF cultures failed to show microorganisms).


High-grade patients are notably predisposed to a number of general complications, often affecting the outcomes. In spite of several cardiac, abdominal, infectious, and respiratory troubles, we did not find a significant influence on either early mortality or six-month GOS. These complications usually occurred in the more compromised patients who were usually those with the larger ICH. Therefore, the ICH volume likely concealed the influence of other factors on the unfavorable results.


Acute hydrocephalus was relatively frequent in this series, but we found no significant association between early ventricular enlargement and the initial GCS, which means that the hydrocephalus played a minor role in sustaining the comatose state of our patients. Moreover, the presence of acute hydrocephalus did image not significantly affect the results, probably because of the early admission and the prompt ventricular drainage in all cases. The vast majority of the survivors with initial hydrocephalus ultimately required a permanent shunt, but the presence of acute hydrocephalus did not result in a significant increase of the risk of chronic hydrocephalus. In any case, most of the survivors required a permanent VP shunt. The routine use of ventricular drainage for ICP management and the frequent presence of intraventricular blood could have led to an increased rate of CSF pathways block. In these particular problematic patients, we found Founder effect difficult to evaluate the actual influence on the outcome exerted by the chronic hydrocephalus. There was no related mortality, but we were not able to quantify the morbidity at least as long as the shunt kept on working correctly.

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