Vascular Injury

The carotid artery enters the cavernous sinus as it exits the foramen lacerum at the base of the skull. It then rises toward the posterior clinoid process before acutely turning anteriorly for approximately 2 cm (the horizontal segment), leaving the cavernous sinus just below the anterior clinoid. There are several small branches of the carotid inside the cavernous sinus, including the meningohypophyseal trunk and the artery of the inferior cavernous sinus. The cavernous sinus itself is an intricate plexus of venous channels surrounding the carotid artery. It lies lateral to the pituitary gland and sphenoid sinus, extending from the superior orbital fissure to the apex of the petrous bone. Among many other venous and sinus connections, the superior and inferior ophthalmic veins and the central retinal artery drain into the cavernous sinus, the former accounting for the exophthalmos and the latter for the possibility of intracranial hemorrhage. The third, fourth, and all three branches of the fifth cranial nerve run within the lateral wall of the cavernous sinus; the sixth nerve passes directly through the sinus alongside the carotid, whereas ocular sympathetic fibers form a plexus on the wall of the carotid.

The classic signs and symptoms of the complete syndrome resulting from CCF include pulsating exophthalmos, a bruit that patients often appreciate, chemosis (conjunctival injection), diplopia, visual loss, and headache. These may evolve over the course of several weeks or months. Their pathophysiologic basis can be deduced readily from the previously described anatomy.

Although a CCF can typically be seen on computed tomography (CT) or magnetic resonance imaging (MRI), angiography is necessary to define the anatomy of the fistula and to identify the associated abnormal venous drainage so as to allow for planning of optimal treatment. Because traumatic CCFs rarely resolve spontaneously, surgical intervention is usually indicated. The timing of intervention depends on the degree and extent of visual loss. Visual deterioration is due to ischemia secondary to increased intraocular pressure and subsequent hypoxia as a result of reduced arterial flow and venous hypertension.

Before the development of endovascular surgical techniques, the most common treatment approach involved occluding the internal carotid artery in the neck as well as intracranially just distal to its exit from the cavernous sinus. Unfortunately, this usually meant sacrificing the ophthalmic artery as well, given its origin just below the anterior clinoid process, with the associated risk of further visual loss.

The current treatment of choice is selective endovascular balloon occlusion of the fistulous connection itself, preserving the carotid artery and its branches. The fistula may be accessed by a variety of routes, including the superior ophthalmic vein, the carotid artery, and the superior petrosal sinus.

Large series of patients with CCFs treated endovascularly have demonstrated a 99% occlusion rate with less than 5% complications.

SECONDARY COMPLICATIONS OF TRAUMATIC BRAIN INJURY

A significant number of patients die or are left severely disabled after TBI, not by the primary injury itself but by the secondary insults that follow. The most common of these are hypotension and hypoxia.

Hypoxia (oxygen saturation less than 90%) and/or hypotension (systolic blood pressure less than 90 mm Hg) was found to occur in greater than one third of patients with severe TBI in the National Coma Data Bank. A single episode of hypotension at any point is associated with a doubling of mortality; of hypoxia with a 33% increase; and the combination with a 75% increase. Thus every effort should be made to prevent or minimize the occurrence of these events.

Another serious secondary insult is intracranial hypertension. It is reasonably well established that maintaining intracranial pressure (ICP) below 20 mm Hg at all times is associated with greater than 90% survival; controlling ICP below this level for greater than 50% of the time is associated with greater than 50% survival; and an inability to ever bring ICP below 20 mm Hg, is accompanied by a greater than 90% mortality.

An important, but still uncontrolled problem is the damaging biochemical cascade that is initiated shortly after injury. The final common pathway to energy failure, and ultimately to cell death, relates to loss of calcium homeostasis and to mitochondrial damage. Opening the cellular membranes to calcium influx is triggered by a variety of mechanisms, including oxygen free-radical production, excitatory neurotoxicity, caspases, and cytokines. The resulting damage may exceed that created by the primary injury. Randomized controlled clinical trials of pharmacologic agents to block this biochemical cascade have not yielded benefit.

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