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Traumatic intracranial aneurysms and fistula associated with epidural haematoma.

has remained well almost a year after his first presentation (fig c). Eleven per cent of extradural haematomata occur in the frontal region and there is experimental evidence to suggest that dural separation may occur at impact with subsequent formation of clots.3 This was probably the mechanism of formation of the first haematoma in the case described. It is the formation of the subdural collection for which there are a number of possible explanations. More than a third of patients with an extradural haematoma have an associated intradural haematoma.1 Delayed intracerebral haematomata are known to occur after evacuation of chronic extracerebral collections. There is probably no single aetiological factor but mechanisms such as focal ischaemia and rapid shift have been implicated.4 In this case, it is unlikely that these mechanisms could be used to explain the formation of a delayed subdural hygroma. The arguments against this would be: (a) no loss of consciousness at presentation, (b) the long duration between injury and presentation of the initial haematoma, (c) no evidence of associated clot or focal damage on the initial scan, (d) the brain remained slack at the end of the first operation with no discolouration of the dura, (e) the patient was neurologically normal immediately after operation for 48 hours. Another possible explanation might be that the dural hitches may have caused cortical or cortical venous injury during insertion. We believe that this was not the case because the patient made a full recovery and was well for the first three days post operatively. The brain showed no signs of injury at the second operation when the dura was widely opened and the cortex inspected; the subdural fluid at the second operation was straw-coloured with no clots or blood seen. The mechanism of formation of this patient's subdural hygroma is obviously a rare one, and probably resulted because of the long duration of contact between the dura and arachnoid, resulting in a tearing of the arachnoid and escape of CSF subdurally on insertion of the "Poppen" suture. A small tear could then have resulted in a "flap valve" mechanism leading to further accumulation of hygroma fluid ultimately causing pressure effects. Because the brain had remained depressed for 48 hours prior to the first operation, we believe that the insertion of the "Poppen" suture resulted in the formation of an ex vacuo subdural hygroma which needed surgical evacuation. When using the "Poppen" suture, we suggest that this possible complication be borne in mind.