Complications of a Giant Cavernous Carotid Artery Aneurysm

Complications of a Giant Cavernous Carotid Artery Aneurysm
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doi: 10.62055/yhpoedqvvgyt

ABSTRACT

INTRODUCTION

Cavernous carotid aneurysms (CCAs) differ from other intracranial aneurysms in that most are asymptomatic and are generally considered benign as there is a low risk of rupture. More common than complications from rupture are complications from the mass effect of the aneurysm itself on nearby structures.1,2 This report describes a case of a giant right CCA that progressed in size despite multiple surgical repairs that resulted in near- complete ophthalmoplegia and neurotrophic keratitis which led to a perforated corneal ulcer and subsequent enucleation.

 

CASE REPORT

An 84-year-old Caucasian man presented to the eye clinic with complaints of diplopia. He was diagnosed with a partial third cranial nerve palsy, and an urgent work-up revealed a 2.5cm giant cavernous right carotid artery aneurysm. He was urgently referred to neurosurgery, who operated twice using endographic stenting, repeated due to complications of recanalization. He diligently went to his scheduled follow ups with his neurosurgeon but returned to the eye clinic with a concern for a change in diplopia. Symptom progression instigated reevaluation which revealed an increase in size of the CCA, now 3.2 cm. He was again referred to neurosurgery who completed a third endographic surgical repair. Nine months after this third repair, he returned to the eye clinic with symptomatic vision loss in his right eye and right orbital pain. Ocular findings suggested a progressed mass effect, now on the second, third, fourth, fifth, and sixth cranial nerves. Additional work-up indicated further progression of his cavernous aneurysm, now 4 cm. He was referred to neurosurgery but did not follow up with this appointment. One week later, he returned to the eye clinic complaining of total vision loss, resulting from an infected corneal ulcer. He was hospitalized to treat this condition, but due to perforation of the cornea, his eye was enucleated on an urgent basis. He was discharged after surgery but unfortunately, he passed away later that day due to delirium complications of a fall, thought to be attributed to his recent vision loss.

 

CONCLUSION

Cavernous sinus aneurysms, while typically benign, can present with multiple ophthalmic complications due to the potential for impact on cranial nerves II, III, IV, V (branch one and two), and VI. Management typically involves frequent monitoring unless complications arise, including pain, double vision, or loss of vision. Cranial nerve V involvement can cause additional ophthalmic complications of severe neurotrophic keratitis and corneal ulceration. Because symptomatic cavernous sinus aneurysms may be neurologically devastating, it is imperative for eyecare professionals to recognize the early signs of a cavernous sinus aneurysm and properly evaluate and refer for treatment and monitoring.

Keywords: Cavernous Sinus Aneurysm, diplopia, corneal perforation, cavernous carotid artery aneurysm, neurotrophic keratitis

 

INTRODUCTION

Cavernous carotid artery aneurysms (CCAs), also called cavernous sinus aneurysms, compose 14% of all internal carotid artery aneurysms. CCAs can arise from trauma, infection, or are idiopathic in origin and are classified according to the size with small domes (<10mm), large (10-25mm), and giant (>25mm).1 CCA differs from other intracranial aneurysms in that most are asymptomatic and are generally considered benign, as there is a low risk of rupture. If rupture does occur, complications include carotid-cavernous fistula, subarachnoid hemorrhage, and epistaxis. More common than complications from rupture, however, are complications directly from the mass effect of the aneurysm itself.1,2 This mass effect may exert pressure on adjacent cranial nerves, commonly the third, fourth, fifth, and sixth cranial nerves. Rarely, cranial nerve II can also be involved.2 This report describes  a case of a giant right CCA that progressed in size despite multiple surgical repairs that resulted in near- complete ophthalmoplegia and neurotrophic keratitis which led to a perforated corneal ulcer and subsequent enucleation.

 

CASE REPORT

An 84-year-old Caucasian man with a history of hypertension and chronic obstructive pulmonary disease presented to the eye clinic with complaints of diplopia. A month prior to this visit, he was diagnosed with restrictive strabismus in supraduction of the right eye following entropion and ptosis repair of the right eye. However, at this following visit, the right eye also had restrictions of adduction, supraduction, and infraduction. Additionally, he presented with moderate neurogenic ptosis of the right upper eyelid, and his right pupil was large and non-reactive and there was no APD by reverse testing. Visual acuities were 20/20 right and left eye. He was diagnosed with a right cranial nerve three palsy and sent to the emergency room for an urgent evaluation. The potential differentials of a cranial nerve three palsy were explored, including giant cell arteritis, vascular etiologies, trauma, intracranial neoplasm, intracranial hemorrhage, and cerebral aneurysm. Trauma was not supported by patient history and ESR, CRP, and CBC were normal. CT and CTA scan revealed a giant intracranial cavernous aneurysm of the right internal carotid artery (Figure 1).

figure 1 cca (1)

Figure 1. CT (inferior coronal view) without contrast showing complex giant intracranial cavernous aneurysm of the right internal carotid artery, measuring 25 mm anteroposterior x 16 mm transverse x 18 mm caudocranial. MRI and MRA of original aneurysm were unavailable for this case report.

 

He was urgently referred to neurosurgery, who operated twice on the aneurysm using endographic stenting. After surgery, he was initiated on anticoagulant therapy to include Plavix 75 mg and aspirin 81 mg daily.  Post-surgical notes indicated that there was an improvement in oculomotor function and pupillary reaction, and the patient was instructed to follow up every six months with neurosurgery with repeat imaging. One year after his second surgical repair and two months after his follow up with neurosurgery, he returned to the eye clinic. His exam demonstrated completely restricted adduction, which prompted obtaining MRI/MRA urgently, which revealed an increase in size of the CCA to 3.2 cm (Figure 2).

figure 2 cca (1)

Figure 2. MRA (inferior coronal view) indicating a giant right cavernous segment internal carotid artery aneurysm, status post endographic surgery, measuring 32 mm anteroposterior x 16 mm transverse x 21 mm caudocranial. Incidentally, there was a second left internal carotid artery aneurysm of the cavernous sinus, measuring 7 mm.

 

The patient was urgently referred back to neurosurgery and underwent a third endographic surgical repair. Post-surgical notes indicated permanent residual oculomotor and pupillary deficits. He was offered an eye patch, but preferred no management of his diplopia, as his ptosis was near complete and prevented symptoms.

Nine months after the third surgical repair, and three months after follow-up with his surgeon, he returned to the eye clinic with vision loss in his right eye and right orbital pain. Visual acuity of the right eye was 20/100 and 20/20 in the left eye. The right pupil was large and non-reactive, though now with an afferent pupillary defect by reverse. Extraocular motility exam demonstrated near complete restriction of all adduction, abduction, supraduction, and infraduction (Figure 3). Additionally, the right cornea had diffuse superficial corneal erosions consistent with the presence of  neurotrophic keratopathy. The neurotrophic component was confirmed by testing corneal sensitivity with a cotton wisp.  Posterior segment examination found new right optic nerve pallor. These combined ocular findings suggested a mass effect on the right second, third, fourth, fifth, and sixth cranial nerves.

figure 3 cca (1)

Figure 3. Photographs demonstrate neurogenic ptosis of the right upper eyelid as well as near total restriction in supraduction, infraduction, abduction, and adduction of the right eye. Photos taken in all gaze viewpoints except for the patient looking up and to his right. Note that photos were taken post-dilation OU.

 

Additional evaluation with urgent MRI/MRA demonstrated further progression of the CCA, now 4 cm anteroposterior. The imaging was taken outside of the facility so only the report was available for review. He was started on aggressive lubrication for his neurotrophic keratopathy and referred urgently to neurosurgery. The patient did not follow up with the appointment with neurosurgery, but he did return back to the eye clinic one week later complaining of complete vision loss in the right eye. Visual acuity was no light perception of the right eye and 20/20 of the left eye. Anterior segment revealed 4+ mucopurulent discharge with a 7x6mm infiltrative corneal ulcer of the right eye. He was immediately transferred and admitted to another hospital to receive fortified natamycin, vancomycin, and gentamycin eye drops every hour, along with oral levofloxacin 20 mg/day. The following morning, his cornea perforated (Figure 4), which led to emergent right eye enucleation.

figure 4 cca (1)

Figure 4: Right eye with dense mucopurulent discharge, conjunctival injection, chemosis, and corneal perforation.

 

A day and a half following the enucleation procedure, he was discharged. Unfortunately, he passed away later that day due to hypoactive delirium complications from a fall, which may have been influenced by his recent vision loss.

 

Discussion

Cavernous sinus aneurysms compose 14% of all internal carotid artery aneurysms and 3-5% of intracranial aneurysms.1 Generally occurring in the elderly, they are most commonly idiopathic, but they may result from trauma or infection.1,2 Infectious CCAs can arise from bacterial, fungal, or viral sources. Infected aneurysms typically present with a fusiform shape as compared to the typical saccular shape.3,4 Cavernous sinus aneurysms involving the internal carotid artery are generally treated as benign, and they present with different risks compared to other types of intracranial aneurysms.1,2 CCAs are surrounded by the cavernous sinus dura, which lies outside of the subarachnoid space. Thus, unlike other intracranial aneurysms, there is a very low risk of subarachnoid hemorrhage, unless the lesion pushes into the subarachnoid space and bleeds.1,2 This occurs in approximately 5% of patients with CCA.5 More commonly, CCA rupture results in a carotid-cavernous fistula; this occurs in about 25% of CCA patients.5 A cavernous sinus fistula may occur if the internal carotid artery atypically connects to the cavernous sinus. This results in the classic triad of pulsatile exophthalmos, chemosis, and ocular bruit.6 Epistaxis, or nosebleed, is another complication of a CCA. This only occurs in 2% of patients, and it requires the aneurysm to grow and hemorrhage into the sphenoid sinus.1,5 Finally, intracerebral hemorrhage, dysarthria, and subdural hematoma may also result from CCA. Most complications, however, arise from a direct mass effect on nearby structures rather than rupture.1

The internal carotid artery travels through the cavernous sinus. An associated aneurysm may cause mass effect on cranial nerves II, III, IV, V (first and second branch) and VI as well as the postganglionic sympathetic plexus (Figure 5).2 Resulting mass effect may cause diplopia from involvement of the cranial nerves innervating extraocular muscles, loss of corneal sensation from involvement of the first branch of cranial nerve V, vision loss from compression of cranial nerve II, facial numbness from involvement of the second branch of cranial nerve V and Horner’s syndrome from involvement of the postganglionic sympathetic plexus. In addition, the mass effect may also cause proptosis, orbital pain, and chemosis.2 A retrospective review of 206 CCAs found 65% presented with diplopia, 59% with pain, and 8% with decreased vision.7

figure 5 cca (1)

Figure 5: Diagram of the cavernous sinus, demonstrating proximity of the internal carotid artery to the following structures: CN II, CN III, CN IV, CN V1, CN V2, CN VI, the sympathetic plexus, the cavernous sinus, and the sphenoid sinus.21

 

 The risk of rupture increases proportionally with the size of the aneurysm.1 Treatment decisions are challenging due to the current lack of evidence-based guidelines.8 Approximately 40% of all CCAs are small.  Small asymptomatic CCAs can be monitored with repeat imaging to evaluate for change over time, as only 2% of these small lesions lead to significant complications.2,8 Surgical treatment should be considered when a patient presents with pain, vision loss, diplopia, or when repeat imaging demonstrates growth that suggests the risk of rupture.2,9 In the past, various surgical methods were used to include bypass techniques, direct clipping of the aneurysm bulb, or occlusion of the feeder vessel.  Currently, CCAs are now preferentially treated with endovascular surgical techniques utilizing stents, balloons, or coils. The overarching goal of surgery is to embolize and preserve the vessel structure, all while minimizing permanent ophthalmological and neurological complications.2,9 The success of endovascular surgery is high, with a 95% 5-year occlusion rate.2  Morbidity from stroke within six months of the procedure is just over 5%.2 Further complications of surgery can include recanalization, as in this case, which can result in the need for repeat procedures.1 Recanalization is a postoperative change demonstrating worsening of an aneurysm occlusion, as blood flow is reestablished into the aneurysm. This occurs in almost half of all giant CCAs.1 Interestingly, giant CCAs may experience spontaneous intramural thrombosis in 13-20% of patients. The theory behind intramural thrombosis is not fully understood, but the feeder vessel to the aneurysm occludes itself, thus eliminating the need for surgical repair.1,9 Accordingly, it is recommended that patients with giant CCAs with mild symptoms or those who have failed previous endovascular surgeries simply monitor their CCA with frequent imaging.9 For this patient, the severity of symptoms caused the patient to elect for surgical repair. Specifically, each of his three surgeries were completed endovascularly using stents to create pipeline flow diversion embolization. Subsequent growth was attributed to recanalization of the ICA. Notably, all stents placed remained patent and without stenosis.

Imaging is the primary mode of diagnosis of CCA, combined with correlation to clinical symptoms.10 The gold standard for cerebral aneurysm detection is digital subtraction angiography (DSA). DSA is not always ideal, however, because of a higher risk of complications compared to other imaging modalities, its cost, and that it is not readily available.10 As a result, CT and CTA imaging are the most common imaging modalities used to diagnose a cerebral aneurysm as they are affordable and able to quickly generate images.8 A CT scan has the advantage over other imaging modalities of assessing if the aneurysm involves local bony structures including the sphenoid bone, as invasion into the sphenoid bone can result in epistaxis. The CTA is needed in addition to the CT to assess the source, flow dynamics, and arrangement of the aneurysm.8 CTA may fail, however, to identify aneurysms whose dome is smaller than 3mm. 10 Compared to CT scans, MRIs are better in identifying any invasion of the aneurysm into the dural space which therefore assesses for risk of rupture leading to subarachnoid hemorrhage. MRA is also more sensitive than CTA, and it can detect small aneurysms less than 3mm.  However, MRA accuracy can be reduced by any vessel or motion artifact.  Despite these important benefits, it can be patient-relevant that MRI and MRAs are more expensive and time consuming.8,10 Despite vulnerability to such artifacts, the improved sensitivity of MRA is recommended over CTA for all patients following endovascular surgery.10

The patient described here initially presented to the eye clinic with signs and symptoms of a partial right cranial nerve three palsy. A month prior to this examination, he was diagnosed with restrictive strabismus following entropion and ptosis repair of the right upper lid. Post-surgical strabismus from lid surgeries is rare. Hayworth et. al., in a retrospective review of 920 blepharoplasties, discovered only three patients with documented diplopia attributed to surgical complications. He hypothesized that swelling and trauma to the muscle sheath of the extraocular muscle caused the diplopia for these three patients.11 A separate retrospective review by Synuita et. al. of 12 patients with post-blepharoplasty diplopia reported each of these 12 patients experienced vertical diplopia.12 Interestingly, this was also the symptom of our patient after his blepharoplasty. Other published case reports of horizontal diplopia following blepharoplasty exist in the literature, and therefore post-surgical diplopia should be evaluated properly as a diagnosis of exclusion.13,14 For this patient, there was no neuroimaging done prior to his lid surgery. His ptosis was attributed to age-related changes, but it is conceivable in retrospect the ptosis was due to the CCA. At his initial presentation to the eye clinic, his new (or possibly progressed) signs of a partial cranial nerve three palsy prompted an urgent referral to the emergency room. Differential causes of cranial nerve IIIpalsy include intracranial neoplasms, intracranial hemorrhages, intracranial aneurysms, trauma, giant cell arteritis, and ischemia due to systemic conditions, most commonly diabetes or hypertension. Urgent work-up for a new onset cranial nerve three palsy should include imaging, such as CTA/CTA or MRI/MRA, and labs for giant cell arteritis (ESR, CRP, CBC). All other cavernous sinus lesions or infections, including neoplasms, fistulas, thrombosis, Tolosa-Hunt syndrome, hemangioma, actinomycosis, and mucormycosis were all ruled out by the patient’s imaging results.2 A CT/CTA was initially performed in this case due to ease of availability, but prior to his neurosurgery, the patient underwent additional MRI/MRA testing. After surgical intervention, the patient later presented with pain, ophthalmoplegia, and reduced acuity, and MRI/MRA imaging showed an associated increase in aneurysm size. It is noteworthy that MRI/MRA were utilized instead of CT/CTA at this time, as they are superior for following aneurysmic changes post-endographic repair.

After his subsequent and third surgical repair, he then presented with neurotrophic keratopathy. Neurotrophic keratopathy eventually led to a perforated corneal ulcer and subsequent enucleation. Neurotrophic keratopathy occurs in approximately 1.6 per 10,000 individuals and is broadly characterized by decreased innervation to the cornea and resultant delayed corneal healing.15 The cornea is innervated primarily by the nasociliary nerve, a branch from the ophthalmic branch of cranial nerve V, and less by the sensory nerves of the maxillary branch of the cranial nerve V. Underlying causes of neurotrophic keratopathy can include recurrent corneal erosion, dry eye, radiation, diabetes, autoimmune diseases, contact lens use, and trauma, but the most common cause remains herpetic keratitis.15 In this case, however, neurotrophic keratopathy was the result of mass effect compression of the ophthalmic and/or maxillary branch of cranial nerve five. What began as stage one keratopathy, with superficial keratitis, quickly developed into stage three neurotrophic keratitis with a large ulcer, further complicated by infection which lead to perforation. As the corneal structure was irreparable and the right eye was blind and painful, this patient was treated with enucleation. After his discharge from his hospital stay, the patient unfortunately passed away from complications of a fall.

In adults over the age of 55, fall-related injuries are the fifth leading cause of mortality.17

Hoffman et. al., in a retrospective review of adults over the age of 65 recently discharged from hospital stays, reported that 14.4% of patients were readmitted within 12 months of discharge, and fall-related injury was the leading cause of readmission.18 Visual impairment is a frequent contributor to falls, and that may have been the case for this patient. Unfortunately, vision as a risk for falls is commonly overlooked due to the lack of guidelines for fall prevention in patients with new onset visual impairment following hospital stays.19 Grievously, this patient fell within 24 hours of discharge. His fall resulted in delirium and subsequently his passing. This highlights a reason why further research should be directed towards the prevention of falls for those with newly acquired vision loss before hospital discharge.

 

CONCLUSION

Cavernous sinus aneurysms of the internal carotid artery are typically considered benign, as there is a low risk of rupture. However, complications, particularly from the mass effect of nearby structures, can be devastating to patients, as they can suffer from facial and ocular pain, diplopia, and vision loss. The management of a cavernous sinus aneurysm is best dealt with an interprofessional team approach, which may include eyecare professionals, neurology, radiology, pain management, and neurosurgery. Management decisions may include close monitoring, treatment of symptoms such as pain, or surgical options. Eyecare professionals should be able to recognize when to evaluate for a potential cavernous sinus lesion and understand  the urgency in which to do so, be aware of  the importance of follow up care, know how to evaluate for potential changes in a cavernous sinus aneurysm, as well as manage any potential ocular complications that may arise.

 

References 

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  2. Seinfeld J, Karim S. Cavernous Sinus Aneurysm. [Updated 2023 May 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430840/
  3. Sacchetti F, Stagni S, Spinardi L, Raumer L, Dentale N, Cirillo L. A singular case of cavernous internal carotid artery aneurysm in patient with cavernous sinus syndrome and bacterial meningitis. Radiol Case Rep. 2016;11(3):227-233. Published 2016 Jun 11. doi:10.1016/j.radcr.2016.05.005
  4. Majeed H, Ahmad F. Mycotic Aneurysm. [Updated 2023 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560736/
  5. Van Rooij WJ, Sluzewski M, Beute GN. Ruptured cavernous sinus aneurysms causing carotid cavernous fistula: incidence, clinical presentation, treatment, and outcome. AJNR Am J Neuroradiol. 2006 Jan;27(1):185-9.
  6. Bowling, B. (2015). Kanski’s clinical ophthalmology: A systematic approach (8th ed.). W B Saunders.
  7. Stiebel-Kalish H, Kalish Y, Bar-On RH, et al. Presentation, natural history, and management of carotid cavernous aneurysms. Neurosurgery. 2005;57(5):850-857. doi:10.1227/01.neu.0000179922.48165.42
  8. Fehrenbach MK, Dietel E, Wende T, et al. Management of Cavernous Carotid Artery Aneurysms: A Retrospective Single-Center Experience. Brain Sci. 2022;12(3):330. Published 2022 Feb 28. doi:10.3390/brainsci12030330
  9. Sastri SB, Sadasiva N, Pandey P. Giant cavernous carotid aneurysm with spontaneous ipsilateral ICA occlusion: Report of 2 cases and review of literature. J Neurosci Rural Pract. 2013;4(Suppl 1):S113-S116. doi:10.4103/0976-3147.116439
  10. Stafa A, Leonardi M. Role of neuroradiology in evaluating cerebral aneurysms. Interv Neuroradiol. 2008;14 Suppl 1(Suppl 1):23-37. doi:10.1177/15910199080140S106
  11. Hayworth RS, Lisman RD, Muchnick RS, Smith B. Diplopia following blepharoplasty. Ann Ophthalmol. 1984;16(5):448-451.
  12. Syniuta LA, Goldberg RA, Thacker NM, Rosenbaum AL. Acquired strabismus following cosmetic blepharoplasty. Plast Reconstr Surg. 2003;111(6):2053-2059. doi:10.1097/01.PRS.0000056840.61348.35
  13. Mazow ML, Avilla CW, Morales HJ. Restrictive horizontal strabismus following blepharoplasty. Am J Ophthalmol. 2006;141(4):773-774. doi:10.1016/j.ajo.2005.11.045
  14. Ortiz-Basso T, Vigo R, Prémoli EJ. Horizontal diplopia following upper blepharoplasty. Case Rep Ophthalmol. 2014;5(3):289-291. doi:10.1159/000367964
  15. NaPier E, Camacho M, McDevitt TF, Sweeney AR. Neurotrophic keratopathy: current challenges and future prospects. Ann Med. 2022;54(1):666-673. doi:10.1080/07853890.2022.2045035
  16. Galor A, Levitt RC, Felix ER, Sarantopoulos CD. Under- standing the true burden of dry eye disease. Expert Rev Ophthalmol. 2015;10(5):403-405.
  17. Patino CM, McKean-Cowdin R, Azen SP, et al. Central and peripheral visual impairment and the risk of falls and falls with injury. Ophthalmology. 2010;117(2):199-206.e1. doi:10.1016/j.ophtha.2009.06.063
  18. Hoffman GJ, Liu H, Alexander NB, Tinetti M, Braun TM, Min LC. Posthospital Fall Injuries and 30-Day Readmissions in Adults 65 Years and Older. JAMA Netw Open. 2019;2(5):e194276. Published 2019 May 3. doi:10.1001/jamanetworkopen.2019.4276
  19. Reed-Jones RJ, Solis GR, Lawson KA, Loya AM, Cude-Islas D, Berger CS. Vision and falls: a multidisciplinary review of the contributions of visual impairment to falls among older adults. Maturitas. 2013;75(1):22-28. doi:10.1016/j.maturitas.2013.01.019
Discover Vision Centers | Leawood, KS

Dr. Cummings graduated from the University of Missouri St. Louis College of Optometry in 2019 and went on to complete a residency in ocular disease and low vision rehabilitation at the Kansas City VA Medical Center. She currently practices at a multi-specialty OD/MD practice in the Kansas City area. Dr. Cummings’ interests include managing glaucoma, retinal vascular disease and ocular manifestations of systemic disease.

Kansas City VAMC | Kansas City, MO

Danielle Toms, OD graduated from NOVA Southeastern College of Optometry in 2014 and completed her residency at the Kansas City VAMC in ocular disease and low vision rehabilitation. She has been employed at the Kansas City VAMC since she completed residency in 2015, starting at the Warrensburg CBOC before moving to the main hospital as the Clinical Lead of the Visual Impairment Services Program. She currently serves as the Clinical Lead of Tele-eye and TECS at the KCVA and is ABO certified.

Kansas City VAMC | Kansas City, Missouri

Dr. Klein graduated from Indiana University School of Optometry and completed a M.S. in Vision Science in 2013. The following year, he completed his residency at the Kansas City VAMC in ocular disease and low vision rehabilitation. He is currently a staff optometrist at the Kansas City VAMC, and is Clinical Lead for Tele-Eye and TECS programs in VISN 15 of the VA.

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