• O Piazza, A Venditto, and R Tufano.
• Department of Anesthesiology and Resuscitation, Federico II University of Naples, Naples, Italy. orpiazza@unina.it
• Panminerva Med. 2011 Sep 1; 53 (3): 203-10.

AbstractAneurysmal subarachnoid hemorrhage (SAH), in addition to the direct effects of the initial hemorrhage and secondary neurological complications, predisposes to medical complications. The proportion of deaths caused by non-neurological medical complications (cardiac, pulmonary, gastrointestinal, renal, hematological) equals that from neurological complications. In particular, pulmonary complications are responsible for 50% of all deaths from medical complications. Neurogenic pulmonary edema (NPE) is an increase of interstitial and alveolar fluid occurring as direct consequence of any acute central nervous system injury. Two different pathogenetic mechanisms of NPE have been hypothesized: i) hemodynamic (an increase of pulmonary vascular pressure due to an α-adrenergic response produces hydrostatic edema) and ii) inflammatory mechanism (brain cytokines and chemokines determinates an increase in the permeability of pulmonary capillaries causing exudative edema). Recent studies postulate that both mechanisms may be implicated in the pathogenesis of NPE. Brain injury is known to determine increased levels of S100B, a Ca- binding protein, in cerebrospinal fluid and in blood. Moreover, amine precursor uptake and decarboxylation (APUD) cells located in the respiratory tract produce and release S100B. This protein may contribute to the pathogenesis of NPE binding RAGE receptors in alveolar epithelial type I pneumocytes and amplifying the immune and inflammatory response causing lung injury. S100B can be the link between the brain and the lung and may be among the multiple pathological pathways that determine the development of pulmonary edema after bleeding.

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