We present an unusual case of cerebellar haemorrhage followed by tension pneumocephalus several days after thoracotomy for resection of a Pancoast tumour. The postoperative course of the 32-year-old patient was complicated by a cerebellar haemorrhage and hydrocephalus caused by compression of the fourth ventricle. Immediate surgical evacuation of the haemorrhage and placement of an external ventricular drain was performed. Respirator ventilation maintaining a continuous positive airway pressure was required. Following weaning and extubation the patient rapidly deteriorated and became comatose. A cranial CT scan revealed a dilated ventricular system filled with air, and air in the subarachnoid space. Recovery of consciousness was observed after aspiration of intracranial air through the ventricular drainage. Recurrent deterioration of consciousness after repeated air aspiration indicated rapid refilling of the ventricles with air.The patient underwent emergency surgical re-exploration of the thoracic resection cavity: dural lacerations of the cervico-thoracic nerve roots C8 and Th1 were identified. Subarachnoid-pleural fistula, cerebellar haemorrhage and tension pneumocephalus after discontinuation of continuous positive airway pressure respiration are unusual complications of thoracic surgery. We discuss the putative pathomechanisms and present a brief review of the literature.

Previous studies have demonstrated that inhibitors of the arachidonic acid metabolism block migration and sensitise human glioma cells to treatment inducing apoptosis. This paradigm may provide a new concept for anti-invasive treatment strategies targeting invasive glioma cells. However, the effect of such treatment on other cellular elements in glial tumours such as endothelial cells is unknown. In this study we have analysed the expression of metabolites of the arachidonic acid pathway in endothelial cells in vitro and in vivo and we have assessed the influence of inhibitors of this pathway on motility, capillary like tube formation, and apoptosis in human endothelial cells. Human endothelial cells (HUVEC) in culture showed expression for thromboxane synthase and both isoforms of cyclo-oxygenase, COX-1 and COX-2. Immunostaining demonstrated low levels of COX-1 expression in capillaries and larger vessels of normal brain and moderately elevated levels of this enzyme in small vessels of brain tumours of various grades. Both thromboxane synthase and COX-2 expression was limited to endothelial cells found in anaplastic gliomas and glioblastomas. Thromboxane synthase inhibitors strongly decreased endothelial cell migration in HUVEC in vitro and capillary like tube formation was strongly inhibited by the compound at a similar dose range. The non-selective cyclo-oxygenase inhibitor ASA and the selective COX-2 inhibitor sulindac only had a minor effect on endothelial cell migration, however, the COX-2 inhibitor sulindac showed a synergistic effect with the thromboxane synthase inhibitor. Thromboxane synthase inhibitors induced apoptosis in endothelial cells as demonstrated by intracellular histone-complexed DNA fragmentation. These data suggest that inhibitors of thromboxane synthase influence migration and apoptosis in both human glioma cells and human endothelial cells. An anti-invasive treatment strategy using this class of compounds may therefore not only sensitise glioma cells to conventional treatments inducing apoptosis but may also be supported by an anti-angiogenic effect.