Guía de actuación clínica en la hemorragia subaracnoidea. Sistemática diagnóstica y tratamiento

Vilalta J. Clinical practice guidelines for subarachnoid haemorrhage.
Diagnosis and treatment. Neurologia. 2014 Dec 16. pii: S0213-4853(14)00220-5.
doi: 10.1016/j.nrl.2014.09.012. [Epub ahead of print] English, Spanish. PubMed
PMID: 25529180.
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¿Es realmente preocupante la hemorragia subaracnoidea traumática?

In 661 patients with isolated tSAH. Only four patients (0.61%) underwent any sort of aggressive neurosurgical, medical, or endovascular intervention, regardless of GCS score. Most tSAH patients without additional systemic injury were discharged home (68%), including 53% of patients with a GCS score of 3-8. However, older patients were more likely to be discharged to a rehabilitation facility (p<0.01). There were six (1.7%) in-hospital deaths, and five patients of these patients were older than 80 years old. Isolated tSAH, regardless of admission GCS score, is a less severe intracranial injury that is highly unlikely to require aggressive operative, medical, or endovascular intervention, and is unlikely to be associated with major neurologic morbidity or mortality, except perhaps in elderly patients. Based upon our findings, we argue that impaired consciousness in the setting of isolated tSAH should strongly compel a consideration of non-traumatic factors in the etiology of the altered neurological status ((Lee JJ, Segar DJ, Asaad WF. Comprehensive Assessment of Isolated Traumatic Subarachnoid Hemorrhage. J Neurotrauma. 2014 Feb 6. [Epub ahead of print] PubMed PMID: 24224706.))

Actualización de la inflamación en la hemorragia intracerebral: sus mecanismos

La inflamación es el factor clave de la lesión cerebral secundaria. La inflamación progresa en respuesta a diversos estímulos.
Los componentes inician la señalización inflamatoria a través de la activación de la microglia, posteriormente la liberación de citocinasproinflamatorias y quimiocinas para atraer la infiltración inflamatoria periférica .
La hemoglobina ( Hb), hemo y el hierro liberado después de la lisis de los glóbulos rojos agravan la lesión inflamatoria.
Las proteínas nucleares de alta movilidad del grupo B1 HMGB1 desencadenan la inflamación en la última etapa 1).

Zhou Y, Wang Y, Wang J, Anne Stetler R, Yang QW. Inflammation in intracerebral
hemorrhage: from mechanisms to clinical translation. Prog Neurobiol. 2013 Nov 26.
doi:pii: S0301-0082(13)00127-5. 10.1016/j.pneurobio.2013.11.003. [Epub ahead of
print] PubMed PMID: 24291544.
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