A 76‐year‐old man presents to the emergency room with right temporal headache and massive epistaxis resulting in cardiovascular collapse requiring cardiopulmonary resuscitation. This event is preceded by a 10‐week history of pounding headache in the right frontal and periorbital area. He then developed diplopia. He was seen by an optometrist and had prism glasses made. He reported that when he lay down, he could hear a pulsatile “whooshing” sound on the right side of his head and around his right ear. Ten weeks earlier, he had a dramatic bout of epistaxis from the right nostril with a large amount of blood pouring from the right nostril into the sink and splashing on the walls in the kitchen. He saw a local ear, nose and throat physician who could not localise the source of bleeding. Initial non‐contrast CT imaging in the emergency department revealed mild scattered microvascular ischaemic changes and no recent infarction or acute intracranial haemorrhage. A high‐density material within the sphenoid sinus and air fluid level in both maxillary sinuses compatible with haemorrhage was noted (fig 1). Neurological examination revealed a left hemiparesis. Examination of the cranial nerve revealed anisocoria with the left pupil greater than the right (5 and 2 mm, respectively) and both unresponsive. Repeat CT and MRI of the head showed new infarcts in the right posterior frontal lobe and patchy areas of the right parietal and occipital lobes consistent with a middle cerebral artery multifocal embolic event. It also showed hyperdense carotid artery in the petrous and cavernous portions consistent with thrombosis. The right superior ophthalmic vein was greater than the left suggestive of a carotid–cavernous sinus fistula (CCF) and impaired venous return in the cavernous sinus. Magnetic resonance angiography of the head revealed occlusion of the right internal carotid artery with otherwise normal intracranial circulation. Neural imaging studies are consistent with a right CCF. The right carotid thrombosis would explain the right middle cerebral artery territory larger infarct seen on neural imaging. As the neurological condition deteriorated, ventilatory support was withdrawn with the expected outcome. He passed away that day.
Figure 1Magnetic resonance angiography showing blood in the maxillary sinuses (arrows).
CCFs are abnormal communications between the carotid artery and the cavernous sinus. Their formation can be spontaneous or post‐traumatic.1
Generally, presentation are unilateral or bilateral exophthalmus, ophthalmoplegia, diplopia and headache. CCFs from cavernous‐carotid aneurysm can be audible pulsatile bruit.2
The CCF may also present with massive and life‐threatening epistaxis.3
Current therapeutic strategies involve percuataneous occlusion of the fistula either by embolisation of feeding arteries transarterially or transvenously by catheterisation of the cavernous sinus.4