On the evening of September 21, 2010 a 60 year old Caucasian female presented to Geisinger Medical Center in Pennsylvania. The oral and maxillofacial surgery service was consulted after the initial evaluation by the emergency room physician. Earlier in the day she was kicked in the face by her horse. She stated that she lost consciousness after the incident but she was not in acute distress and was awake, alert, and oriented. The patient had an unknown medical history and could not remember the medications she was taking. She denied past surgical history and she said that she had no known drug allergies. The patient denied tobacco use and admitted to being a social drinker. The patient denied any nausea or vomiting, dizziness, changes in vision or hearing, and numbness or tingling of her extremities. Her lungs were clear to auscultation bilaterally and her heart had a regular rate and rhythm, with palpable peripheral pulses present, and no murmurs were auscultated. The patient had no tenderness across her thoracic or lumbar spine. The patient had a c collar placed and her neck was immobilized as per advanced trauma life support protocol until x rays confirmed no concomitant spinal injuries.
She complained of “right eye pain and a loose mandible.” The patient presented with an 8.5 cm laceration across her right cheek. Additionally, she had an obvious deformity of her mandible. Her pupils were 3 mm, bilaterally reactive to light, with extraocular muscles intact. She denied diplopia and did not have subconjunctival hemorrhage, but did have mild right periorbital edema and ecchymosis. She had no gross hearing impairment and no discharge was observed from her ears. The patient’s nose had no epistaxis and was not deviated. The patient had facial nerve weakness on the right side demonstrated by the patient’s inability to move her lips on the right side. She also presented with a deviation of her mandible to the right side upon opening. Her mandible had a step defect in the region of the right premolars. The patient had a laceration through the buccal mucosa in the region of the right maxillary tuberosity. Intraorally, the parotid salivary flow through stenson’s duct on the right side had active salivary discharge upon palpation. She had no floor of the mouth swelling and no tongue elevation.
Initially, the patient was given morphine as need for pain and unasyn 1.5 grams every 6 hours. Her open right facial laceration was loosely approximated in preparation for surgical repair.
A maxillofacial computed tomography (CT) scan without contrast was taken as shown in figures 1 and 2. The patient was found to have multiple complex facial fractures including a grossly comminuted right mandible angle fracture with gross displacement as well as a grossly comminuted right zygomatic complex fracture and severe orbital floor fracture extending posteriorly near the orbital apex.
Due to the acute nature of the injury and gross contamination of the wound with all fracture sites being open through the cheek wound, it was decided she should be taken to the operating room the next day for surgical repair and reduction of the fractures with debridement of the wound. The right facial wound measured approximately 8 cm in length and was through-and-through and communicated to the intraoral cavity. The right zygomatic complex fracture as well as the right mandibular fracture was both visible through the wound. Both fracture sites were able to be accessed through the wound. The laceration had communicated intraorally in the region of the parotid duct. The parotid duct was evaluated, inspected, and probed; and it did not appear that the parotid duct was violated or lacerated. The facial laceration had extended proximal to the lateral canthal region and primary repair of the facial branches of cranial nerve VII were not able to identified or repaired. There was gross comminution of the mandible fracture. The mandible was able to be reduced primarily. There was no visualization of the inferior alveolar nerve. Once the mandible had been adequately stabilized and reduced, a locking reconstruction plate was adapted to the right inferior border extending from the right angle anteriorly to the right mandibular body region. The plate was secured with 12 mm screws. There was adequate stability of the mandibular fracture after placement of the plate. The right zygomatic complex fracture was then addressed. The zygomatic complex was noted to be grossly comminuted with shattering of the right anterior maxillary sinus wall. A Carol Gerard screw was placed into the malar eminence region in order to be used as traction to reduce the right zygomatic complex in order to obtain correct anterior-posterior protection. The right zygomatic arch was also reduced with a Dingman elevator. Once the zygomatic arch was brought into proper position, an extended maxillofacial reconstruction plate was adapted from the right zygomatic buttress region anteriorly to the right piriform rim region. This was secured with 6 mm screws. There was also gross displacement of the inferior orbital rim; therefore, a transconjunctival incision was made in order to access the right inferior orbital rim as well as the right lateral orbital rim. A right lateral canthotomy incision was also made in order to access the right lateral orbital rim. Once the inferior orbital rim was approached, the periosteum was incised with Bovie cautery and the right inferior orbital rim and lateral rim were able to be exposed with the periosteal elevator. There was no dissection performed along the right orbital floor as there was gross comminution of the floor, however, no gross entrapment was visualized radiographically. The right infraorbital rim was able to be primarily reduced and stabilized with a straight maxillofacial plate and secured with 6 mm screws. At this point, the right lateral rim was also identified and appeared to be primarily reduced. Therefore, no plate was placed at the right lateral rim. Her occlusion was stable and repeatable after she was released from fixation and the mandible had been plated. A forced duction was performed, and there appeared to be no entrapment and adequate mobility of the extraocular muscles. The patient was admitted postoperatively for continued observation and care.
Post operative day one, the patient was in stable condition with swelling and discomfort consistent with the surgery that was performed. As shown in figure 3, a post operative CT was taken. The CT demonstrated posttraumatic facial contusions and postsurgical facial edema and intraorbital fat stranding/edema with moderate right orbital proptosis.
2 days status post facial fracture reduction and laceration repair, the patient presented with pain around her right eye with severe proptosis, chemosis, and limited visual acuity. The patient was evaluated by ophthalmology. Her right eye visual acuity was difficult to assess but she was able to count fingers with the right eye. Her intraocular pressure (IOP) was 28 in the right eye and 12 in the left eye. IOP lowering eye drops were given at bedside (timolol x 2, xalatan x 1, iopidine x 3). The patient was also started on decadron 8mg IV q 8 h for 24-36 hours. She was also placed on diamox (acetazolamide) 500 IV one dose and she was started on cosopt (dorzolamide hydrochloride-timolol maleate) 1 drop in the right eye BID. The ophthalmologist felt that her right eye vision was likely reduced and hoped that reducing IOP with the above medications would prevent further visual loss.
3 days status post surgery, the patient was evaluated again by the ophthalmology department. Her IOP was noted to be 25 in the right eye and 14 in the left eye. Her pupils were equally round and reactive to light with accommodation (PERRLA), with no relative afferent pupillary defect (RAPD) and no anisocoria. Her lateral canthal sutures were removed to help relieve pressure. Her right upper eyelid was mobile and her lower lid was tense. The patient had limited ductions of the right eye with notable chemosis and edema. It was recommended that the patient have ice water compresses, decadron 8mg Q8h x 3 days, maxitrol ophthalmic ointment QID to the right eye, and continuation of cosopt. The patient’s bed was also elevated 30 degrees.
4 days status post surgery, the patient was evaluated by the surgical trauma and ophthalmology because she reported progressive decreased vision out of her right eye and was in a considerable amount of pain. Her IOP was back up into the mid 30s on repeat evaluations. Diamox IV 500 BID was continued. A paracentesis was done at bedside with 0.1cc removed. Decadron 8mg q6h was recommended because any further orbital swelling may cause further damage. A CT of the orbits was ordered promptly for evaluation as shown in figure 4. The CT demonstrated a right zygomaticomaxillary complex fracture with retrobulbar fat stranding similar to the prior CT scan, with likely resolving hemorrhage. There was an asymmetric prominence of the right superior ophthalmic vein, stable since prior exam. Also noted was fullness and increased density in the region of the right cavernous sinus. These findings raised concern for a possible carotid-cavernous fistula. Vascular congestion or thrombosis was also considered in the differential diagnosis.
Later that same day, a superior cantholysis was performed in the ophthalmology clinic. Figures 5 and 6 represent pictures taken after the cantholysis was done. Significant bleeding was produced during the procedure. Following the procedure her pain level improved but she still could not see well out of her right eye. The motility of her right eye was almost frozen. Her sclera was white and her cornea was clear. Her right eye also demonstrated a resistance to retroplusion with a positive demarcation line of erythema. Also, a harsh orbital bruit was heard when the bell of a stethoscope was placed on her right eye. The ophthalmologist advised to stop the decadron and to start solumedrol 1 g over 1 hour for 3 doses. According to the clinical examination and later confirmed by the radiologist, it was likely that the patient had a carotid cavernous fistula and this would explain why there was no response to steroid therapy. The patient’s case was discussed with the hospital’s interventional neuroradiologist, and a MRI, MRV, and MRA were promptly ordered. Her vision remained guarded and the patient was scheduled for an angiogram the following day. Her thyroid studies and coagulation profile were both within the normal limits.
The MRI scan of the orbits without and with intravenous contrast and MR angiogram and MR venogram of the brain was done as shown in figures 7-9. Sagittal T1-weighted images of the entire brain were obtained. Thin axial pre-and post contrast images were acquired through the orbits including axial and coronal T1 and T2 and axial and coronal fat-suppressed post gadolinium T1-weighted images. These scans demonstrated mild to moderate right proptosis. Right preseptal and periorbital soft tissue edema was identified. The right globe was intact and demonstrated normal morphology. Mild edema was detected in the retrobulbar fat. Mild edema and enlargement of the right extraocular muscles was seen. Small likely hemorrhagic fluid collection was noted in the superior extraconal space of the right orbit. The right superior ophthalmic vein was moderately enlarged with likely arterialized flow. The right cavernous sinus appeared mildly enlarged as well. The left orbital contents were unremarkable. Visualized portions of the brain demonstrated mild generalized cerebral parenchymal atrophy. A focal T2 hyperintensity in the right frontal deep white matter was nonspecific and possibly represented chronic small vessel ischemic changes. No other significant abnormalities were detected in the visualized portions of the brain. The midline structures including the pituitary gland, corpus callosum, brainstem, pineal region and craniocervical junction were unremarkable. Hemorrhagic fluid was seen in the right maxillary sinus and anterior ethmoid air cells. Mucosal thickening was noted throughout the right-sided paranasal sinuses. Arterialized flow was suspected in the right cavernous sinus extending into the right superior ophthalmic vein; findings were most consistent with traumatic carotid cavernous fistula. All intracranial arterial vessels in the bilateral carotid and vertebrobasilar circulation, including right cavernous carotid artery, demonstrated normal course, caliber, outline, and branching pattern without evidence of stenosis, dilatation or aneurysm. Prominent right posterior communicating artery was seen. Aside from the above described right cavernous sinus and superior ophthalmic vein, all imaged intracranial venous structures including dural venous sinuses, deep venous structures and cortical veins demonstrated normal course, caliber and branching pattern without evidence of stenosis or thrombosis.5 days status post surgery, the patient still had pain associated with her right eye, proptosis and poor vision in her right eye. Due to the presence of a carotid cavernous fistula her vision prognosis remained poor. As per neurosurgery the plan was for urgent evaluation and treatment of the patient’s carotid cavernous fistula. A cerebral angiogram was first performed before actual treatment in order to assess the anatomy and to make a plan for definitive treatment of the fistula. This uncomplicated cerebral angiogram demonstrated a direct right carotid cavernous fistula with extensive flow in the superior ophthalmic vein anteriorly and the cavernous sinus and internal jugular vein on the ipsilateral side as well as the sigmoid sinus posterolaterally as shown in figure 10.
The following day transarterial and transvenous partial treatment of the patient’s right direct cavernous carotid fistula was accomplished as shown in figure 11. Transarterial treatment consisted of telescoping Wingspan microstent and the transvenous treatment consisted of cavernous sinus coil embolization. The result was slowing of the persistent fistula. Further embolization in two weeks was planned if the patient remained stable and her intraocular pressures continued to decrease. However, if the patient’s symptoms worsened, the plan was to proceed with immediate embolization and possible carotid sacrifice.
1 day status post intracranial stenting right internal carotid artery (ICA) and transvenous coiling in right cavernous sinus, the patient’s IOP decreased to the lower 20s. The patient’s right eye appeared less swollen, but still slightly proptotic and tight. The patient still had minimal light perception. The patient was told that her vision may not improve.
2 days status post treatment of CCF, the patient’s right eye presented with no pain and she stated that she can see "bubbles of light." She also reported still hearing a mild "whooshing" sound in her right ear that had been present since her eye symptoms began. Upon examination it was determined that she had no light perception despite her subjective feeling above. Her right pupil was 6 mm and nonreactive. The patient demonstrated no motion in any direction with her right eye. It was determined that her fistula was still present but it slowed down, should slow down more, and was trending in right direction. Her IOP was now 20 mmHg and stable. The patient was discharged at this point.
Two weeks later the patient presented with a traumatic carotid cavernous fistula status post partial traumatic direct carotid cavernous fistula right side; status post subtotal treatment transarterially and transvenously. The plan now was for a second procedure approaching from the left to access the anterior cavernous sinus via the circular sinus as there was no direct access via the ipsilateral vein at the time of the initial treatment. Treatment of the right direct carotid cavernous fistula using a transvenous approach from the left cavernous sinus via the left inferior petrosal sinus was done. This performed a coil embolization as shown in figure 12. There was complete cessation of retrograde flow into the superior ophthalmic vein and small amount of flow in the cavernous sinus.
The patient was evaluated by neurology and ophthalmology 1 month later status post coil occlusion of her right direct CCF. This had no clinical complications. The patient presented with an improvement of her symptoms but she did mention that she hears a little whooshing from time to time. This has not gotten worse and her symptomatology has not returned. Her edema was much improved; the patient had limited motility in the lateral and superior gazes. Her vision remained poor as the patient could only see shadows and blurred colors. A follow up angiogram to assess occlusion of her right CCF will be done in 6 months. An angiogram will be done sooner if the patient's symptoms become more progressive or get worse.
According to a pubmed literature search, a carotid cavernous fistula has never been reported associated with trauma caused by a horse. It is important to realize the possible lethal power of a horse which is capable of delivering a kick with a force of up to one ton. Horseback riding accidents and injuries caused by horses carry a high risk of severe trauma. In addition, a horse’s kick can transfer a force of more than 10 000 Newtons to the body, causing fractures of the skull or other bones as well as devastating damage to the intestines.[i] Additionally, horses are large and fast, often weighing 450 kg (1000 pounds) or more and travelling up to 30 mph with the rider’s head over 9 feet above the ground.[ii] Even when not mounted on a horse, a person can be seriously injured because a horse’s kick can generate a force up to 1.8 times its body weight.[iii] Most horse related injuries occur among females, which is in contrast to other injury causes which are often more prevalent for males.[iv]
The development of a CCF is a rare complication of craniofacial trauma, reported to occur in only 0.17% of cases.[v] Benjamin Taverns first described this condition in 1809 as unilateral pulsating exophthalmos in a patient who subsequently lost vision in the affected eye.[vi] CCFs can be divided in direct and indirect types. A direct fistula results from a hole in the cavernous portion of the internal carotid secondary to trauma or, less commonly, a congenital weakness in the vessel wall. In contrast, the indirect fistula is a dural arteriovenous fistula involving the cavernous sinus and the ICA, the external carotid, or both.[vii] Compared with direct CCFs, indirect CCFs have a more gradual onset, usually with a milder clinical presentation.
The schema developed by Barrow and his colleagues7 in 1985 based on angiographic
studies is the most commonly utilized. According to their system, there are four types of CCF. Type A (direct) involves a shunt between the ICA and cavernous sinus and is typically associated with trauma and produces early signs and symptoms. Type B (indirect) involves a shunt between the meningeal branches of the ICA and the cavernous sinus. Type C (indirect) involves a shunt between the meningeal branches of the external carotid artery and the cavernous sinus. Lastly, type D (indirect) involves a shunt between the meningeal branches of the ICA, external carotid artery, and the cavernous sinus.
To understand the pathphysiology and treatment of CCFs, the oral and maxillofacial surgeon must been very familiar with the anatomy in the region. The cavernous sinuses are a paired structure, 2 cm long and 1 cm wide, within the sphenoid bone in the anterior portion of the middle cranial fossa.6 The cavernous sinuses communicate with each other via the anterior and posterior intercavernous sinus, also known as the circular sinus. The anatomy of the cavernous sinus is unique because it is the only anatomic location in the body in which an artery travels completely through a venous structure.6 Because the ICA is fixed to the surrounding dura of the base of the skull, it is exposed to shearing forces and penetrating injuries. The ICA is anchored at its entrance and exit from the sinus. The internal carotid artery lies on the medial wall of the cavernous sinus with the abducens nerve in close proximity. The oculomotor, trochlear, and the ophthalmic and maxillary divisions of the trigeminal nerve are located adjacent to the lateral wall of the cavernous sinus within its dural walls. The abducens nerve is most vulnerable because, unlike the other nerves, it courses freely in the sinus without a protective dural covering.6 The cavernous sinus essentially functions as a dural venous structure, receiving blood supply from the superior and inferior ophthalmic veins as well as from the sphenoparietal sinuses. Also, there are venous communications with the opposite cavernous sinus, the clival venous plexus and the transverse sinus.
There have been reports of traumatic, spontaneous, and iatrogenic causes of CCFs. The traumatic type is caused by severe head injury after a high velocity traffic accident, major skull base fracture or penetrating injury through the orbit. The spontaneous type can be congenital, secondary to rupture of a carotid aneurysm into the cavernous sinus or acquired with multiple arterial branches of the carotid arteries that shunt into the cavernous sinus. The later type is found more commonly and has been referred to as dural CCF.[viii] Spontaneous CCFs typically result from a ruptured carotid aneurysm. However, some authors have suggested that this fistula formation has been associated with fibromuscular dysplasia, collagen vascular disease, Ehlers-Danlos syndrome, antherosclerotic vascular disease, and hypertension or straining.[ix] There are many reported iatrogenic causes of direct CCF, including Le Fort I osteotomy, maxillectomy, orbital floor fracture repair, septorhinoplasty, cataract surgery, carotid endarterectomy, Fogarty catheter thrombectomy, nasopharyngeal biopsy, myringotomy, and sphenoethmoidal surgery.[x]
Although penetrating cranial injuries can cause CCF, severe blunt trauma is the more common mechanism. Traumatic forces associated with severe head trauma and fractures can cause the internal carotid artery to be torn from its dural attachments and rupture, thus leading to direct flow into the cavernous sinus. The flow between the high-pressure internal carotid artery and the low pressure of the cavernous sinus results in relatively high pressures in the sinus, impeding venous drainage from the orbit and compressing the vital structures within it. A CCF can occur at five specific areas along the course of the ICA in the cavernous sinus.[xi] These include the anterior ascending segment of the ICA, the junction of the anterior ascending and horizontal segments, the horizontal segment of the ICA, the junction of the horizontal and posterior segments, and the posterior ascending segment. In general, CCFs are more commonly associated with anterior tributaries of the cavernous sinus than with posterior tributaries.[xii] This congestion created within and around the cavernous sinus explains the clinical symptoms and possible unfavorable outcomes of CCF.
The onset of initial clinical presentation of a traumatic CCF is unpredictable; onset may occur within a few hours to 1 yr after injury.[xiii] Symptoms develop suddenly in direct fistulas that can
occur days or even weeks after head injury.[xiv] The classic triad of physical signs are chemosis, pulsatile exophthalmos and ocular bruit. [xv] Reduced visual acuity, proptosis, ptosis, prominent facial veins, edema of periorbital tissues, diplopia, ophthalmoplegia, papilloedema, increased intraocular pressure, retinal hemorrhage and optic atrophy may be present as well. A case of CCF with lethal epistaxis has also been reported.[xvi] Loss of vision and, on rare occasions,
death can result from acute subarachnoid or intracerebral hemorrhage or cerebral infarction.[xvii]
Chemosis. or severe edema of the conjunctiva, occurs from high venous pressure that causes diminished tissue fluid reabsorption.[xviii] Visual impairment can result from retinal ischemia due to a reduced ocular perfusion pressure. Ptosis can occur from disruption of innervation to the levator palpebrae superioris muscle and of the sympathetic innervation to Mueller’s muscle.[xix]
The oral and maxillofacial surgeon must understand and thereby rule out other conditions that present with similar signs and symptoms as CCF. The differential diagnosis for CCF should include superior orbital fissure syndrome, orbital apex syndrome, orbital hematoma, vascular lesions such as arteriovenous malformation, cavernous sinus thrombosis, cavernous sinus tumors, orbital tumors, skull base tumors and mucocele. The only relevant clinical test confirming the diagnosis of CCF is that the bruit should stop with digital compression of the ipsilateral carotid artery in the neck.[xx] A thorough clinical examination, proper and timely use of imaging, and prompt request for appropriate specialist consults will enable the clinician to make the correct diagnosis.
The definitive diagnosis of a CCF fistula relies on the gold standard, carotid angiography. Angiography best characterizes the flow rate of the fistula and clearly distinguishes between direct and indirect fistulas, showing the exact anatomic location of the ICA tear versus dural feeders of the ICA or external carotid artery (ECA). It also aides in assessing the draining venous pathways (anterior vs. posterior), cortical venous reflux, venous stenosis, or occlusions that could limit transvenous access into the cavernous sinus.[xxi] Contrast CT and MRI help to generate the diagnosis and to demonstrate peripheral pathologies such as proptosis, enlargement of the superior ophthalmic vein, and swelling of extraocular muscles. They are noninvasive forms of imaging but limited by the inability to show precise filling of the cavernous sinus. CT with contrast can also demonstrate any bony fractures/spicules around the cavernous sinus as well as outlining engorged superior ophthalmic veins, a common radiographic finding in CCF.[xxii]
Ultrasound shows similar findings as the CT and MRI. It demonstrates the reversal of blood flow in the superior ophthalmic vein. Chen and his colleagues from Taiwan retrospectively reviewed 53 cases in which CCF proven on digital subtraction angiography (DSA) was compared with CT
angiography (CTA) and MR angiography (MRA). They found a valuable diagnostic role for CTA and MRA, with CTA comparable to DSA in selective cases as a diagnostic tool for CCF.[xxiii]
The goal of treatment in direct CCFs is to occlude the site of communication between the ICA and the cavernous sinus while preserving the patency of the ICA. Currently, treatments most commonly utilized include transarterial obliteration of the fistula with a detachable balloon, deployment of a covered stent across the area of the fistula, or obliteration of the ipsilateral cavernous sinus with coils or other embolic material. If the defect is large and cannot be repaired, the ICA may have to be sacrificed or trapped. [xxiv] Serbinenko revolutionized the therapy for
CCF in the 1970s by introducing detachable intravascular balloons. Endovascular detachable balloon occlusion of CCF introduced through a transfemoral access allows preservation of the distal aspect of the ICA, thereby reducing morbidity.[xxv] Definitive treatment of CCF is usually performed by interventional radiologists or neurologic surgeons as in the case presented. In the modern era, neuroendovascular therapy offers a safe and effective treatment for patients with CCF and has replaced open surgery as the treatment of choice. Recently, Gralla et al.[xxvi] have reported on the use and efficiency of the Amplatzer vascular plugs in their series of 4 patients. Their experience suggested that these plugs may have potential for occlusion of large vessels and high-flow lesions in neuro-intervention. Navigation, positioning and detachment of the device were satisfactory in all of their cases. Untreated CCF can lead to visual loss secondary
to retinal hypoxia and optic nerve atrophy, subarachnoid hemorrhage, glaucoma, cataract formation, neurologic deficit, seizure, and fatal epistaxis.[xxvii] Indirect fistulas have a better chance of closing without vascular intervention by spontaneous thrombosis because of the lower pressure flow. Some studies show that repeated, intermittent carotid compression performed by patients may be used to successfully close these fistulas.[xxviii]
CCF is a well-known disease entity that can be encountered in daily clinical practice. CCF can cause visual and neurological deficits when the condition is left untreated. The ultimate and definitive treatment of a CCF typically falls beyond the scope of oral and maxillofacial surgery. However, clinicians treating patients with craniofacial injuries should have a complete understanding of this pathological entity, because urgent intervention may improve patient outcome. Early recognition by the oral and maxillofacial surgeon and prompt treatment modalities can significantly reduce the morbidity and mortality associated with CCF.
It is a diagnosis to consider in all cases of painful eye symptoms and visual disturbance both at the time of injury and in the days and weeks that follow the initial trauma. As demonstrated by the case presented, optimal management of CCF requires multi-disciplinary collaboration between neurologists, neurosurgeons, neuroophthalmologists and interventional neuroradiologists in order to ensure optimal outcomes. The case presented was unusual because the patient suffered a CCF as the result of a horse kick. The carotid artery may have been damaged in the neck by the sudden, forceful extension of the neck or turning of the head to the contralateral side as a result of the horse kick.[xxix] The shearing forces of severe head trauma and fractures can cause the internal carotid artery to be torn from its dural attachments and rupture, thus leading to direct flow into the cavernous sinus. The patient’s outcome in this case may have been improved by an earlier diagnosis with appropriate ophthalmic and neurosurgical referrals once there was a high index of suspicion for a CCF. This may have led to a delayed radiological embolization. Early diagnosis confirmed by angiography is essential for appropriate treatment and prevention of permanent sequelae.
Figure 1: Coronal CT demonstrating facial fractures at initial presentation.
Figure 2: 3D reconstruction of CT scan demonstrating grossly comminuted right mandible angle fracture as well as a grossly comminuted right zygomatic complex fracture and severe right orbital floor fracture extending posteriorly near the orbital apex
Figure 3: Axial CT taken s/p ORIF demonstrating postsurgical facial edema and intraorbital fat stranding and edema with mild right orbital proptosis
Figure 4: Axial CT taken 4 days s/p ORIF demonstrating moderate proptosis and there was an asymmetric prominence of the right superior ophthalmic vein, stable since prior exam. Also noted was fullness and increased density in region of right cavernous sinus
Figure 5: Photograph s/p cantholysis demonstrating edematous, ptotic, and proptotic right eye.
Figure 6: Photograph s/p cantholysis demonstrating edematous, ptotic, and proptotic right eye.
Figure 7: MRI scan of the orbits
Figure 8: MRA Angiogram
Figure 9: MR venogram
Figure 10: Initial cerebral angiogram demonstrating a direct right CCF with extensive flow in the superior ophthalmic vein anteriorly and the cavernous sinus and internal jugular vein on the ipsilateral side as well as the sigmoid sinus posterolaterally
Figure 11: Angiogram following transarterial treatment consisting of telescoping Wingspan microstent and transvenous treatment consisting of cavernous sinus coil embolization
Figure 12: Angiogram following treatment using transvenous approach from the left cavernous sinus via the left inferior petrosal sinus. A coil embolization is demonstrated.
[i] Chitnavis JP, Gibbons CL, Hirigoyen M, et al: Accidents with horses: What has changed in 20 years? Injury 27:103–5, 1996
[ii] Watt GM, Finch CF: Preventing equestrian injuries: locking the stable door. Sports Med 22:187–97, 1996
[iii] Kriss TC, Kriss VM: Equine-related neurosurgical trauma: a prospective series
of 30 patients. J Trauma 43:97–9, 1997
[iv] Vyrostek SB, Annest JL, Ryan GW: Surveillance for fatal and nonfatal injuries– United States, 2001. MMWR 53:SS1–57, 2004
[v] Arseni C, Ghitescu M, Cristescu A: Traumatic carotid cavernous fistulas. Psychiatry Neurol Neurochem 73:237, 1970
[vi] Niamtu J, Campbell RL: Carotid cavernous fistula. J Oral Maxillofac Surg 40:52-56, 1982
[vii] Barrow D, Spector R, Braun I, et al: Classification and treatment of spontaneous carotid-cavernous fistulas. J Neurosurg 62:248, 1985
[viii] Cheng KM, Chan CM, Cheung YL: Transvenous embolisation of dural carotid-cavernous fistulas by multiple venous routes: a series of 27 cases. Acta Neurochir 145:17-29, 2003
[ix] Uehara T, Tabuchi M, Kawaguchi T, et al: Spontaneous dural carotid cavernous sinus fistula presenting isolated ophthalmoplegia: evaluation with MR angiography. Neurology 50:814-816, 1998
[x] Fattahi T, Brandt M, Jenkins S, et al: Traumatic Carotid-Cavernous Fistula: Pathophysiology and Treatment. J Craniofac Surg 14:2, 2003
[xi] Debrun G, Lacour P, Vinuela F, et al : Treatment of 54 traumatic carotid-cavernous fistulas. J Neurosurg 55:678–692, 1981
[xii] Mohyuddin A. Indirect carotid cavernous fistula presenting as pulsatile tinnitus. J Laryngol Otol 114:788–789, 2000
[xiii] Takenoshita Y, Hasuo K, Matsushima R, et al: Carotid Cavernous sinus fistula accompanying facial trauma. J Cranio-Max-Fac Surg18:41 -5, 1990
[xiv] Mostafa G, Sing RF, Matthews BD, et al: Traumatic carotid cavernous fistula. J Am Coll Surg
[xv] Iida K, Kurisu K, Arita K, et al. Critical Cerebral Ischemia Revealed by Magnetic Resonance Imaging in a Traumatic Carotid-Cavernous Fistula without High-Risk -Patterns on Angiograms: A Case Report. J Trauma 53:109- 11, 2002
[xvi] Borba R, Sonda I, Dini LI, et al : Carotid-cavernous fistula with lethal epistaxis: case report. Arq Neuropsiquiatr 59:276-9, 2001
[xvii] Fabian TS, Woody JD, Ciraulo DL, et al. Posttraumatic carotid cavernous fistula: frequency analysis of signs, symptoms, and disability outcomes after angiographic embolization. J Trauma
[xviii] Wilkins R. Rengarchy S, Eds. Carotid-cavernous fistulas and intracavemous aneurysms. Neurosurgery. New York: McGraw Hill; 1483-94, 1985
[xix] Sanni K, Campbell R, Rosner M, et al: Internal carotid arterial occlusion following mandibular osteotomy. J Oral Maxillofac Surg 42:394. 1984
[xx] Pothula VB, Reddy KT, Nixon TE. Carotico-cavernous fistula following septorhinoplasty. J Laryngol Otol 113:844–846, 1999
[xxi] Gemmete J, Chaudhary N, Pandy A, et al: Treatment of Carotid Cavernous Fistulas. Current Treatment Options in Neurology 12:43–53, 2010
[xxii] Hu WY, Hudon M. Neuroimaging highlight: traumatic carotid- cavernous fistula. Can J Neurol Sci 27:71–72, 2000
[xxiii] Chen CC, Chang PC, Shy CG, et al: CT angiography and MR angiography in the evaluation of
carotid cavernous sinus fistula prior to embolization: a comparison of techniques. Am J Neuroradiol 26:2349-56, 2005
[xxiv] Debrun G: Treatment of carotid cavernous fistula using detachable balloon catheters. AJNR Am J Neuroradiol 4:355, 1983
[xxv] Serbinenko FA. Balloon catheterization and occlusion of major cerebral vessels. J Neurosurg 41:125–145, 1974
[xxvi] Gralla J, Schroth G, Kickuth R, et al: Closing the gap between coil and balloon in the neurointerventional armamentarium? Initial clinical experience with a nitinol vascular occlusion plug. Neuroradiology 50:709–14, 2008
[xxvii] Lewis AI, Tomsick TA, Tew JM. Management of 100 consecutive direct carotid-cavernous fistulas: result of treatment using detachable balloons. Neurosurgery 36:239–246, 1995
[xxviii] Higashida RT, Hieshima GB, Halbach VV, et al: Closure of carotid cavernous sinus fistulae by external compression of the carotid artery and jugular vein. Acta Radiol Suppl 369:580 –583, 1986
[xxix] Lanigan D, Tubman D: Carotid-cavernous sinus fistula following Le Fort I osteotomy. J Oral Maxillofac Surg 45:59, 1987