Introduction 

   An injury of the intracavernous carotid artery occurs in 1 patient out of 10,000 hospital admission due to trauma.¹³⁾ A connection between the ICA and one of the adjacent intracavernous veins will result in a CCF. A pseudoaneurysm will develop if the arterialized rent from the injured ICA flows directly into the bare perivenous spaces within the cavernous sinus, without a shunt with one of the veins. A CCF and a pseudoaneurysm can be present in the same patient.¹³⁾ But there are very rare, we experienced successful endovascular treatment case of combined lesion. So we report our experience and literature review. 

Case Report 

   A 24-year-old man was admitted with headache, mental deterioration, right hemiparesis and left exophthalmos. He had had head trauma history 5 years ago, and then a computed tomographic (CT) scan had revealed anterior fossa basal skull fracture and the presence of intracranial air. On this admission, CT scan revealed spontaneously developed intracerebral hemorrhage (ICH) on frontal and temporal lobe, intraventricular hemorrhage and basal cistern subarachnoid hemorrhage. Cerebral angiography was performed to evaluate the cause of his symptoms and intracranial hemorrhage. Carotid angiography revealed a CCF associated with about 17x15mm sized pseudoaneurysm on the C3 portion of left ICA (Fig. 1). We decided to occlude the ICA at the level of pseudoaneurysm because of its large vascular wall defect; multiple fistulous opening; communication with posterior circulation; high rupture risk (ruptured capsule not enough to support the artery and pseudoaneurysm). Collateral circulation was evaluated prior to definitive carotid occlusion using a BTO. 
   A bilateral transfemoral approach was done using Seldinger's technique. The cervical ICA was catheterized with a 7.5 F guiding catheter (Envoy ; Cordis Corp., Miami, FL) and a microcatheter and Hyperform balloon (4mm in diameter and 7mm in length, MTI) were introduced coaxially. The inflated balloon was then propelled by blood flow proximal to the entrance of the C3 ICA aneurysm, where the parent vessel was occluded. Angiographic cross flow studied were performed via a 5.5 F catheter positioned in the contralateral ICA and left vertebral artery. The patient did not undergo a continuous peri- and postoperative heparinization due to ICH resulted from rupture of CCF. During BTO, the ICA stump was flushed 3~5 times with heparinized saline (1000 IE/10ml) in addition to continuous rinsing of all catheters with haparinized saline (1000 IE/1000ml). Tolerance to test occlusion was assessed by a detailed neurological examination consisting of evaluation of cranial nerve function, muscle strength and language ability every 5 minute. He clinically tolerated the 20 minutes of BTO under normotension. During BTO, angiography revealed a symmetric angiographic filling of both hemispheres. After then, hypotension was induced by the infusion of sodium nitroprusside. After the mean arterial pressure was reduced to two thirds of baseline, hypotension was maintained for 15minutes. During induced hypotensive challenge test with BTO, he clinically tolerated the procedure and there was no definite angiographic change compared with the result of normotensive BTO. A microcatheter (Prowler-14 ; Cordis Corp., Miami, FL) was carefully navigated through the C3 portion of the ICA. Complete occlusion of ICA at the site of pseudoaneurysm was achieved using 31 Gulielmi detachable coils (GDCs) of different sizes. During the permanent occlusion, the balloonassisted deployment was not required. 
   After the permanent occlusion of left ICA (Fig. 2), the perfusion CT was taken. The Perfusion CT revealed no perfusion defect (Fig. 3). His headache and left exophthalmos improved, but his left vision didn't improve. He was discharged without any other complication. Three months after the procedure, the patient's neurological condition greatly improved. He was alert and his right hemipasresis was recovered fully. 

Discussion 

   The classic symptom triad of pseudoaneurysm presents with severe epistaxis, unilateral loss of vision and fracture of the cranial base.⁴⁾ 
   In the present case, the pseudoaneurysm was formed at the junction of the C3 portion of the ICA, and there was a direct fistula into the cavernous sinus. This form of CCF is rare, but Fu et al. reports in the literature of four similar cases with intradural ICA pseudoaneurysm.¹⁰⁾ These cases were treated by trapping of the ICA, neck clipping of the pseudoaneurysm, and transarterial balloon embolization, respectively.^15)19)26) Three possible mechanisms may explain the occurrence of a traumatic aneurysm of the intradural ICA after a nonpenetrating head injury : 1) direct injury to the ICA caused by cranial base fractures, 2) injury caused by overstretching or torsion of the carotid siphon after movement of the brain during the impact of head injury, and 3) injury caused by collision of the ICA with the adjoining bony prominence.⁸⁾¹⁹⁾

   Pseudoaneurysms differ from other aneurysms because there is no true wall. Many treatment strategies have been used in the management of pseudoaneurysms, including observation. 
   Surgical treatments for pseudoaneurysms have involved direct clipping, wrapping, trapping, and carotid artery ligation.⁵⁾ Surgical treatment of a posttraumatic aneurysm is difficult because of its fragile fibrous wall and broad neck.^2)6)8)25)32) There is a risk of hemorrhage and ischemia in clipping this kind of aneurysm.⁸⁾ Considering this risk, some authors prefer ligation of the parent artery.²⁵⁾³²⁾ Even in posttraumatic aneurysms, some authors consider neck clipping while retaining the patency of the parent artery as an ideal treatment modality.^6)19)22)26) To circumvent a premature aneurysm rupture, some authors took the following precautions: 1) the cervical ICA was exposed, 2) a Heifetz encircled clip was kept handy for use in case of perforation of the ICA, and 3) the superficial temporal artery was preserved during the scalp exposure.¹⁰⁾ Preoperative hemodynamic parameters, such as the results of a BTO or cerebral blood flow, are helpful for planning surgical and endovascular strategy.¹⁰⁾ Although carotid occlusion technique is a simple and effective treatment for the aneurysm itself, the outcome mainly depends on the patients' long-term tolerance to permanent carotid occlusion.¹⁷⁾ 
   Endovascular techniques for BTO of parent vessels have been developed to assess the vascular reserve of a particular vascular territory with neurologic monitoring before arterial sacrifice.²⁹⁾ Abrupt carotid artery occlusion is associated with a neurologic ischemic rate of 49% for ICA ligation and 28% for common carotid artery occlusion, as reported in the Cooperative Study of Intracranial Aneurysm and Subarachnoid hemorrhage,²¹⁾³¹⁾ whereas after a clinically tolerated test occlusion, the rate varies from 5% to 20%.⁷⁾¹²⁾ 
   In an effort to reduce this morbidity, several investigators have used one or more of the following additional tests, estimating the effect of BTO on CBF directly or indirectly during BTO : stable Xe CT, 133Xenon single photon emission CT (SPECT), 99mTc hexamethylpropylene amine oxamine (HMPAO) SPECT, H2O positron emission tomography (PET), electroencephalography (EEG), and transcranial Doppler ultrasonography (TCD).³⁰⁾ Each method has its advocates, but none, as yet, has been shown to predict delayed cerebral ischemia after permanent carotid occlusion in all patients.⁹⁾ 
   Linskey et al. promoted the use of stable Xe CT to predict outcome after carotid artery occlusion.¹⁷⁾ Low-risk patients was defined as patients with blood flow greater than 30mL/100g per minute during BTO. However, Origitano et al. reported a rate as high as 22% for delayed neurologic deficits after negative BTO with SPECT.²³⁾ In addition, the need to transport patients with balloons in the ICA to inflate and deflate without constant fluoroscopic control may increase the risk of complications.²⁹⁾ 
   TCD allows a non-invasive continuous beat by beat hemodynamic analysis of the collateral function.¹¹⁾²⁸⁾ ICA sacrifice is feasible when test occlusion results in an ipsilateral initial reduction in VMAC(Velocity of middle cerebral artery) A to 60% of pre-occlusion values.²⁷⁾ TCD analysis of the first cardiac cycles following carotid artery occlusion carries a high sensitivity (86%), specificity (93%) and positive predictive value (86%) compared to 30~45min BTO with neurological surveillance.¹¹⁾²⁷⁾ 
   EEG is often used in monitoring during carotid endarterectomy, but its use during test occlusion in selected patients for definitive carotid occlusion has been poorly studied.³⁰⁾ In one series of nine patients who underwent occlusion after testing with EEG monitoring, cerebral infarction occurred in both patients with EEG changes during BTO, but also in one with normal EEG findings during BTO.²⁰⁾ 
   Angiographic evaluation of the venous phase symmetry between the occluded and the injected territories can predict the safety of permanent ICA occlusion.¹⁾ Angiographic analysis during BTO is ultimately one simple method to measure the redistribution of blood flow. Abud et al. suggests that permanent ICA occlusion will be safe when venous drainage delay in the BTO is not >2 seconds. In patients with venous drainage delay of 2~4 seconds, the ICA occlusion is recommended only in selected cases, because of the impossibility to predict ischemic events.¹⁾ 
   It has been suggested that performing a controlled pharmacologic hypotensive challenge during BTO of the ICA may be a simple provocative test to determine if adequate collateral compensation has occurred during the test study.¹⁴⁾ Origitano et al. reported that 4(22%) of 18 patients undergoing endovascular carotid occlusion with negative normotensive BTO experienced delayed ischemic deficits.²³⁾ According to Standard and his colleague, the addition of hypotensive challenge lowers the rate to 5%.²⁹⁾ 
   If parent vessel occlusion is contemplated in a patient with suspected limited cerebrovascular reserve, the surgeon should prepare for a bypass procedure.²⁹⁾ 
   Another concern of ICA occlusion, is a theoretical risk of developing de novo aneuryms on the contralateral ICA or vertebrobasilar system, because of increased hemodynamic stress exerted on the remaining vessels.⁴⁾ 
   With advances in endovascular technology and devices, preserving patency of the ICA as far as possible is a more desirable goal.³⁾ The choice of endovascular carotid stent placement combined with GDCs has been advocated.³⁾ However, aneurysmal thin fibrin capsule may not offer enough support to the artery and pseudoaneurysm. There is a possibility of progressive enlargement and development of a new psudoaneurysm.³⁾ Recently, there were several reports of using the covered-stent, which is more flexible and selfexpandable.³⁾¹⁸⁾ It is covered on both the luminal and abluminal sides with highly porous polytetrafluoroethylene, which may decrease distal embolization during stent deployment by trapping debris, as well as serving as a physical barrier to prevent neointimal proliferation and restenosis.¹⁸⁾ Ideally, covered stents may play an important role in the occlusion of CCFs with preservation of the parent artery, however they are not yet widely available and are associated with some problems such as acute thrombosis.¹⁶⁾ 
   At sometimes an unexpected pseudoaneurysm was shown to due to obliteration of CCF.²⁴⁾ While performing cerebral angiography in patients with a CCF, vertebral angiogram with manual compression of both ICAs may show aneurysm from the posterior communicating artery and fistulous drainage into the cavernous sinus. 

Conclusion 

   There are many treatment strategies in the management of pseudoaneurysm combined with CCF. Preoperative evaluation, consists of neurologic monitoring for 20 to 30 minutes in combination with one or two additional tests, estimating the hemodynamic or electrophysiologic effect of ICA occlusion, is necessary for planning surgical and endovascular strategy and coping with unexpected vascular insult. Evaluation of the vascular reserve can reduce the mortality and morbidity after permanent carotid occlusion. 

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