|Year : 2022 | Volume
| Issue : 2 | Page : 133-139
Management of neurovascular emergencies with ophthalmic manifestations
Jawahar Lal Goyal, Shalini Singh, Sarvesh Chandra Mishra, Shipra Singh, Divya Singh
Department of Ophthalmology, School of Medical Sciences and Research, Sharda University, Greater Noida; Department of Radiodiagnosis, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
|Date of Submission||14-Jul-2021|
|Date of Decision||07-Aug-2021|
|Date of Acceptance||24-Mar-2022|
|Date of Web Publication||29-Jun-2022|
Dr. Shalini Singh
New Colony, Krishna Bihari Nagar, Fatehpur, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Patients with neurovascular disorders sometimes approach the ophthalmologists with mild ophthalmic clinical features such as conjunctival congestion, slowly progressive proptosis, lateral rectus palsies and at other times with ophthalmic emergencies like sudden increase in proptosis, ophthalmoplegia, diplopia, and ptosis before the onset of neurological manifestations which may be life-threatening if not detected in time. The aim of this article is to focus on ophthalmic manifestations of neurovascular emergencies and role of ophthalmologists in its management. In this communication, to make the ophthalmologist aware of clinical presentations, the imaging modality of choice, diagnostic features, medical and interventional treatments. We have searched PubMed, Web of Science, Google Scholar and reviewed some of the commonly encountered neurovascular emergencies with ocular manifestations such as carotid-cavernous fistula, cerebral venous sinus thrombosis, cerebral artery aneurysms, arterio-venous malformations.
Keywords: Carotid-cavernous fistula, cavernous sinus thrombosis, cerebral aneurysm, neurovascular emergency, ophthalmic manifestations
|How to cite this article:|
Goyal JL, Singh S, Mishra SC, Singh S, Singh D. Management of neurovascular emergencies with ophthalmic manifestations. Oman J Ophthalmol 2022;15:133-9
|How to cite this URL:|
Goyal JL, Singh S, Mishra SC, Singh S, Singh D. Management of neurovascular emergencies with ophthalmic manifestations. Oman J Ophthalmol [serial online] 2022 [cited 2022 Aug 15];15:133-9. Available from: https://www.ojoonline.org/text.asp?2022/15/2/133/348981
| Introduction|| |
Neurovascular emergencies require timely assessment and management to ensure the best clinical outcome. Patients with neurovascular disorders approach to the emergency department with sudden onset of hemiparesis, quadriparesis, multiple cranial nerve palsies, subarachnoid hemorrhage (SAH), or epidural hemorrhage. Conditions such as carotid-cavernous fistula (CCF), cavernous sinus thrombosis (CST), brain arteriovenous malformations, and cerebral aneurysms with or without rupture, can have an acute presentation with initial ophthalmic manifestations. Understanding these life-threatening neurovascular conditions clinically is essential for the ophthalmologist. In this article, we have aimed to discuss and review the important neurovascular emergencies of the brain with regard to their clinical presentations, imaging modalities, diagnostic features, and medical and interventional management and outcome. We have searched the electronic databases, i.e., PubMed, Web of Science, and Google Scholar. Data were pooled and narrative synthesis was conducted.
| Carotid-Cavernous Fistulas|| |
CCFs are direct shunts from the cavernous portion of the internal carotid artery (ICA) into the cavernous sinus. CCFs are spontaneous, but the majority occur after traumatic injury to the ICA or its branches. Road traffic accidents are the most common form of inciting agent and predominantly involve the male population. Iatrogenic interventions such as internal carotid endarterectomy, trans-sphenoidal resection of a pituitary tumor, maxillofacial surgery, and percutaneous treatment of trigeminal neuralgia are less common but still important.
A CCF is an abnormal vascular connection between arteries and veins of the cavernous sinus. CCFs may be classified into two types based on communication: Direct fistulas (Barrow type A) and indirect or dural, fistulas (Barrow types B, C, and D).
Direct fistulas are formed by a direct connection between the ICA and the cavernous sinus. They are commonly high-flow fistulas. Blunt injury or aneurysmal rupture of ICA aneurysm with in cavernous sinus can cause the direct fistula.
Indirect or dural carotid-cavernous fistulas are typically low-flow fistulas that are formed by communications between the cavernous sinus and cavernous arterial branches. Barrow type B fistulas involve meningeal branches of the ICA, Barrow type C consists of external carotid branches, and type D fistulas consist of meningeal branches from both the external and internal carotid arteries. The most commonly involved branch of ICA, is the inferior cavernous branch. Causes of indirect fistulas include Ehlers-Danlos syndrome More Details, hypertension, fibromuscular dysplasia, and dissection of the ICA.
Patients with carotid-cavernous fistula complain of visual blurring, headache, diplopia, ocular pain, and subjective bruit. CCF formation causes arterialization of the ophthalmic venous system, resulting in immediate obvious orbital congestion [Figure 1]a. Arterialized venous system elevates intraocular pressure, causes weakness and limitation of movements of extraocular muscles, proptosis, arterialization and dilation of conjunctival vessels, chemosis, and venous retinopathy.
|Figure 1: (a) Congestive changes with proptosis in carotid-cavernous fistula. (b) Computed tomography showing proptosis (denoted by thin white arrow) and hemosinus (denoted by thick white arrow). (c and d) T2 images showing dilated superior ophthalmic vein (denoted by thick white arrow in c and thin white arrow in d) and enlarged cavernous sinus (denoted by thin white arrow in c). (e) Digital subtraction angiography showing steal phenomenon, fistula site (denoted by thick black arrow) and dilated superior ophthalmic vein (denoted by thin black arrow) are seen. (f) Digital subtraction angiography showing fistula obliteration using balloon (denoted by thin white arrow)|
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Cranial and sympathetic neuropathy, secondary to CCF or due to the direct effect of trauma can be seen. Isolated third nerve or sixth nerve or combination of third, fourth, and sixth nerve dysfunction is common. Arterialization of the ophthalmic vein causes increased episcleral venous pressure, leading to secondary glaucoma. At least 20% of patients will develop glaucomatous visual field defects. If IOP is high enough it can lead to central retinal artery occlusion (CRAO).
The presence of orbital bruits is highly suggestive of high flow shunt. If the proptosis is subtle then the condition can mimic chronic conjunctivitis. The presence of bright red limbal loop vessels will be highly suggestive of carotid-cavernous fistula. However in chronic conjunctivitis, conjunctival vessels appear darker and do not have loops near the limbus. In CCF, the fundus will show dilated and engorged retinal veins, retinal hemorrhages of venous retinopathy. Optic disc swelling is common. Orbital bruits that are heard by both examiner and patients are more prevalent in high-flow fistulas. Low-flow CCF patients will have only subjective bruits.
Ultrasonography shows signs of abnormal hemodynamic connections in the orbit. Abnormal superior ophthalmic vein (SOV) will appear as dark, curved sonolucent tubular shadow, superior-medial to the optic nerve. High flow of ophthalmic vein is better demonstrated on Doppler ultrasonography.
Computed tomography (CT) reveals enlargement of the ophthalmic venous system, more common in the superior division. Proptosis, orbital congestion, and swelling of soft tissues, particularly extraocular muscles will be evident. CT images may reveal other sequelae of head injury in traumatic CCF cases [Figure 1]b.
Magnetic resonance imaging (MRI) is not essential if CT has been performed in traumatic CCF patients. Findings of MRI are often similar to CT in most cases. However, the high flow of arterialized veins will be better appreciated [Figure 1]c and [Figure 1]d.
In CT angiography or digital subtraction angiography, direct CCF will show immediate opacification during the arterial phase of injection. Retrograde flow from the cavernous sinus to ophthalmic veins might be seen, especially in SOV [Figure 1]e.
The use of 3D rotational angiography permits the identification of fistula with detailed anatomic characterization. However, selective cerebral angiography is the diagnostic modality of choice.
The primary goal of therapy is to occlude the abnormal arterio-venous (AV) blood shunting and to regain the normal blood flow.
Spontaneous closure is unlikely and can be considered in low-flow fistulas. Manual carotid compression of involved ICA may be attempted in low-risk fistulas, with approximately 30% success rate in low-flow fistulas and relatively less in high-flow fistulas.
In cases of proptosis with severe exposure, glaucoma or optic neuropathy, emergency closure of CCF is necessary. Emergency embolization should be done within 1 week of severe symptoms. Percutaneous embolization via arterial route is performed through the femoral artery. When the catheter with a detachable balloon, is reached to the fistula site, high flow of shunt carries the partially inflated balloon attached catheter into and through the shunt [Figure 1]f. When the balloon reaches the venous side of the fistula, the balloon is inflated and detached from the catheter. The catheter is then removed.
Transvenous approach via inferior petrosal sinus, superior petrosal sinus, pterygoid plexus, inferior ophthalmic vein, or SOV is still preferred. During the transvenous approach, a catheter is inserted through the internal jugular vein and inferior petrosal sinus. The direct orbital approach can be considered in cases with difficult transvenous access, with an approximately 90% success rate without major complications. Detachable balloons, metal coils, cyanoacrylate can be used for thrombosis. Coils commonly are used in the transvenous procedure. Nylon-fibred platinum coils are better than bare platinum coils because of their improved thrombogenicity. When an embolization is not feasible then stereotactic radiosurgery, cervical ligation of the Common Carotid Artery (CCA), ICA, or surgical interventions may be considered as an alternative treatment.
| Dural Venous Sinus Thrombosis|| |
Thrombosis of the dural venous sinus is frequently overlooked, except when there is the involvement of cavernous sinus. The findings are related to the location of the involved sinus and secondary thrombosis or occlusion of adjacent cortical and subcortical veins. Septic thrombus develops in conjunction with an infection of adjacent structures like paranasal sinuses or meninges. Aseptic thrombosis is rare and occurs in chronic debilitating conditions such as carcinoma or chronic lung conditions.
Cerebral venous thrombosis
Cavernous sinus thrombosis
When CST is associated with traumatic carotid-cavernous fistula or dural AV malformation, it is rarely life-threatening. In contrast, if the thrombosis is associated with a septic process, the consequences can be catastrophic. Previously, septic CST resulted from oral, nasal, or facial bacterial infection that propagated intracranially along the venous connections or directly from adjacent structures. The use of antibiotics has significantly decreased this etiology. At present, fungal invasion from adjoining paranasal sinuses or hematogenous routes are predominant causes of septic thrombi, especially in immunocompromised patients. Rarely, orbital cellulitis-associated thrombophlebitis in the ophthalmic vein can directly lead the infection into the cavernous sinus.
Clinical signs and symptoms develop as a result of congestion in the ophthalmic venous system and damage to local cranial nerves of the cavernous sinus and superior orbital fissure. The patient complains of headache, nausea, and vomiting because of increased intracranial pressure and fever, chills and tachycardia because of septic thrombus.
Patient will also complain of orbital pain, diplopia, proptosis and red eye because of increased orbital venous pressure. On examination patient will have lid edema, chemosis, congestion and hyperesthesia of ophthalmic division of trigeminal nerve. Partial or complete ophthalmoplegia and ptosis are out of proportion to the amount of orbital congestion. 6th nerve involvement is the initial neurological sign. Although the clinical findings begin in the ipsilateral side of the orbit, thrombosis can extend to the opposite side of the cavernous sinus via intracavernous connection and leads to the development of proptosis and lid edema on the contralateral side.
Venous stasis retinopathy, CRAO, ischemic optic neuropathy and extension of infection into the optic canal causing optic neuritis, all can lead to visual loss. Orbital congestion may lead to mark elevation of intraocular pressure which further causes ischemic optic neuropathy or retinopathy and decreased pupillary reaction.
CT should be done urgently to confirm the diagnosis. Contrast films may show enlargement of the cavernous sinus. SOV may appear enlarged and tortuous. Soft-tissue changes, including opacification of adjoining paranasal sinuses and inflammation of the mucosal layer, can be evident. If the infection has reached the orbit, both extraconal and intraconal soft tissue changes, usually next to the affected sinus, with extraocular muscle enlargement may be noticed.
MR is the imaging study of choice to investigate a patient suspected of having CST. CT venography or MR venography can be considered for a detailed dural venous sinus study. If the clinical suspicion is very high despite normal CRV or MRV, cerebral venography is advised to confirm the diagnosis.
Immediate treatment with appropriate intensive high dose intravenous antibiotics should be started, considering suspected causative organisms. Blood and paranasal sinus samples should be sent immediately for gram stating, KOH mounting, culture, and sensitivity testing. Corticosteroids are needed if phlebitis affects the pituitary gland, but if a fungus is the inciting agent, corticosteroids predispose to the spread of infection. The role of anticoagulation in CST remains controversial. The use of low-dose heparin seems to be of very little value. Warfarin can raise the prothrombin times as high as three times of normal which leads to an increased risk of cerebral hemorrhage. Early complete heparinization decreases the morbidity of survivors but does not seem to alter the mortality rate. surgical drainage of the involved paranasal sinus may be needed to decrease the infective load.
Lateral (transverse) sinus thrombosis
Septic sinus thrombosis can occur following otitis media. Patients with lateral sinus thrombosis present with fever, chills, and other systemic signs of sepsis. Postauricular edema, pain over the neck area, and tenderness in the ipsilateral jugular vein may be present. Involvement of the 5th nerve can cause severe facial pain, when accompanied by 6th nerve palsy, it is called Gradenigo's syndrome.
Urgent CT or MRI [Figure 2]a should be advised. CR venography may be needed. If clinical suspicion is high despite normal CRV or MRV [Figure 2]b, then cerebral venography can be considered to confirm the diagnosis. Site, size, and location can be confirmed after cerebral venography and needed intervention should be performed accordingly.
|Figure 2: (a) T1-weighted axial postcontrast images of brain showing filling defect in right transverse sinus suggestive of thrombosis (denoted by white arrow). Please note associated distension suggesting acute nature. (b) Contrast-enhanced magnetic resonance venography showing nonvisualization of right transverse sinus consistent with thrombosis|
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Carotid cavernous aneurysm
It is an extradural aneurysm of the cavernous segment of the ICA. It predominantly causes neuro-ophthalmic symptoms.
Clinical symptomatology is similar to the dysfunction caused by mass effect in the cavernous sinus. It typically presents as diplopia, ptosis, blurred vision, orbital and facial pain, and lateral rectus paresis of the involved side. Rupture of aneurysm can lead to sudden worsening of signs and symptoms. If the aneurysm is colossal then it can extend into optic foramen and patients can develop optic neuropathy. The diagnosis of the cavernous ICA aneurysm can be made on CT [Figure 3]a.
|Figure 3: (a) Noncontrast Computed tomography showing partially thrombosed aneurysm from left cavernous internal carotid artery (denoted by white arrow). (b) T1 postcontrast image showing aneurysm. (c) Digital subtraction angiography image of left cavernous internal carotid artery showing aneurysm (denoted by white arrow). (d) Digital subtraction angiography image showing flow diverter device (denoted by white arrow) in left cavernous internal carotid artery reducing flow to aneurysm|
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MR is the best noninvasive imaging modality to visualize an aneurysm and its relation to the ICA [Figure 3]b. It may readily be used to know the extent to aneurysm to intradural space or into the optic foramen. Better detailing like origin and extent of cavernous aneurysm is decided by cerebral angiogram [Figure 3]c.
Treatment is indicated if there is continuous progressive vision loss or debilitating cranial neuropathy is seen. Endovascular coiling, ballooning, and flow diversion [Figure 3]d are established techniques for the treatment of cavernous carotid aneurysms (CCAs). Catheter with a detachable balloon is inserted through the femoral artery. Entrance and exit of ICA from the aneurysm and ICA at the level of aneurysm are also blocked by one or more detachable balloons. Clipping of aneurysm in cavernous sinus may be attempted if embolization cannot be performed.
Posterior cerebral artery aneurysm
It is commonly present at the origin of the posterior communicating artery from the ICA and comprises approximately 39% of all ruptured intradural aneurysms.
Patients generally present with clinical manifestations of SAH with concomitant involvement of the third cranial nerve. Pupil involving oculomotor nerve paresis is more common with, and suggestive of unstable posterior communicating artery aneurysm and needs to be evaluated urgently. Posterior communicating artery aneurysm rarely extends anterolaterally to compress Chiasm or optic tract. In these cases, Visual field loss will be asymmetrical and will typically cause Central or temporal scotoma ipsilateral to aneurysm.
PCA aneurysm is difficult to diagnose with CT [Figure 4]a, [Figure 4]b, [Figure 4]c or MRI [Figure 4]d until it is very large. In most cases, cerebral angiography [Figure 4]e is needed to establish the diagnosis. If untreated 60% of ruptured PCA aneurysm rebleed within 6 months.
|Figure 4: (a) NCCT brain showing aneurysm at internal carotid artery bifurcation (denoted by blue arrow). (b) Computed tomography angiography showing aneurysm at internal carotid artery -Posterior communicating artery junction (denoted by blue arrow). (c) Magnetic resonance angiography showing aneurysm (denoted by blue arrow). (d) Postcontrast magnetic resonance imaging showing coil mass in aneurysm (denoted by blue arrow). (e) Digital subtraction angiography showing aneurysm (denoted by blue arrow). (f) Digital subtraction angiography (postcoiling) showing coil mass in aneurysm (denoted by blue arrow)|
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Surgical clipping has been considered the first treatment modality. If clipping has not been possible in previously explored aneurysms, then percutaneous embolization [Figure 4]f can be done. Cervical carotid ligation is considered as an alternative if the previous two procedures cannot be performed.
Carotid ophthalmic artery aneurysm
It consists of about 13% of all intracranial aneurysms and 20% of them have bilateral aneurysms. Approximately 31% to 64% of the cases have additional aneurysm in other sites of the brain. It frequently impairs the function of the anterior visual pathway and therefore holds a significant importance in ophthalmology.
The most common clinical presentation is SAH. Patients experiencing visual loss have a lower incidence of SAH. Progressive visual disturbances are more common in the ruptured aneurysm (around 60%).
Despite the proximity of aneurysm to optic nerve and chiasm, headache and orbital pain, rather than visual loss are the most common complaints in these patients. This Slowly enlarging aneurysm causes gradual diminution of vision until there is the involvement of other eyes. Giant aneurysm, if crossed the midline, may compress the contralateral optic nerve or optic chiasm or both.
Visual field loss can be variable and will depend on the involvement of the respective part of the anterior visual pathway. Insidious and gradually progressive visual loss can be misdiagnosed as normal-tension or low-tension glaucoma. However, the visual field loss will be asymmetric and optic disc findings also will not correlate to the corresponding field or vision loss.
CT will not be able to differentiate the aneurysm from tumor. If a bitemporal field defect is present then misdiagnosis of pituitary tumor or pituitary apoplexy is possible. Fluid void within the aneurysmal lumen is diagnostic of aneurysm and can be demonstrated in MRI.
There are two schools of thought about the management of unruptured aneurysm. Some authors suggest close follow-up visits, others have advised to clip or embolize the aneurysm if possible.
| Arteriovenous Malformations|| |
AV malformations are usually congenital or familial. About 90% of them are supratentorial and the remaining 10% are located in the posterior fossa. Supratentorial AV malformations can be cortical (70%) or deep (20%).
Clinical deficits depend on the age of the patient when the clinical symptoms begin and the area of the brain involved. Cortical malformations in the occipital lobe may develop visual symptoms and headache, visual phenomena are unformed and brief. Hemispheric AV malformation may produce hemianopic field defects. Clinical symptoms of brainstem A-V malformations are nonspecific and include nystagmus, diplopia, anisocoria, oculomotor nerve palsy, pupillary light near dissociation, and gaze palsy.
Patients can remain asymptomatic for years or can present with headache, diplopia, blurred vision, or focal or diffuse neurologic dysfunction. These patients frequently complain of tinnitus, audible bruit, and clinical manifestations of increased intracranial pressure like headache, vomiting, and papilledema. Dural AV malformations are difficult to diagnose with routine imaging studies and may be mistaken for idiopathic intracranial hypertension (IIH). Catheter angiography Should be performed if the patient does not fit into IIH demographics.
CT [Figure 5]a and MRI [Figure 5]b and [Figure 5]c scans can demonstrate the AV malformations. Anatomical location and feeding, nidus, and draining vessels of AV malformation can be demonstrated in cerebral angiography [Figure 5]d. Surgical resection, ligation, and embolization [Figure 5]e of feeding vessels are treatment modalities which can be used alone or in combination.
|Figure 5: (a) NCCT brain showing lesion (denoted by white arrow) in the occipital lobe. (b) T1 image showing lesion (denoted by white arrow). (c) T2 image showing flow (denoted by white arrow) voids within lesion suggesting pial arteriovenous malformation. (d) Digital subtraction angiography image showing pial AVM. (e) Digital subtraction angiography image postembolization showing the onyx cast (denoted by black arrows). Note made of microcather (denoted by yellow arrow)|
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| Conclusion|| |
For proper management of neurovascular emergencies, a multidisciplinary approach involving an ophthalmologist, radiologist, neurologist, and neurosurgeon is a must. Early diagnosis and management will definitely improve patient outcome.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]