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| Lot Number UNKNOWN |
| Device Problem
Adverse Event Without Identified Device or Use Problem (2993)
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| Patient Problems
Ischemia (1942); Necrosis (1971); Loss of Vision (2139)
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Event Type
Injury
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Manufacturer Narrative
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Company comment: the serious events of blindness unilateral, ophthalmic artery occlusion, ophthalmoplegia, optic ischaemic neuropathy, anterior segment ischaemia, retinal ischaemia and implant site necrosis were considered expected and possibly related to the treatment.Seriousness criteria included the need for multiple medical interventions and permanent damage.The non-serious, expected events of erythema, swelling and haemorrhage at implant site, cutaneous contour deformity, eyelid ptosis, enophthalmos, strabismus, papilloedema, corneal oedema, conjunctival oedema, retinal oedema, choroidal effusion and the unexpected events of lagophthalmos, madarosis, hypotony of eye, corneal erosion, pupillary reflex impaired, conjunctival hyperaemia, iris atrophy, atrophy of globe, retinal degeneration and vitreous detachment were considered possibly related to the treatment.Iris atrophy, atrophy of globe, retinal degeneration and vitreous detachment were considered to be secondary events of the ophthalmic artery occlusion.The potential root cause include intravascular filler injection leading to vascular occlusion and its manifestations.Potential contributory factors include injection technique and treatment performed by a non-medical practitioner.The case meets the criteria for expedited reporting to the regulatory authorities.Final manufacturer comment: routine investigations have been performed and provide sufficient information to assess the potential root cause and indicate a possible association to the treatment procedure.Lot number was not reported and the product could not be verified.The information in this case does not indicate a non-conforming product or malfunction.The performed investigations are therefore considered adequate and no additional investigations will be conducted.Capa comment: no corrective or preventive actions are deemed necessary based on the outcome of the performed investigations.
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Event Description
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Case reference number (b)(4) is a literature report identified on 06-apr-2022 during literature search.This case refers to a 43-years-old caucasian female patient.This case was identified from the literature article davidova p, muller m, wenner y, konig c, kenikstul n, kohnen t.Ophthalmic artery occlusion after glabellar hyaluronic acid filler injection.American journal of ophthalmology case reports 2022;26:101407.Abstract: a healthy, 43-year-old woman underwent her first hyaluronic acid injection in the glabella and went blind on her left eye immediately thereafter.The massaging of the injection area and observation were performed, before she presented with swelling of the left forehead and upper lid, ptosis, complete ophthalmoplegia and blindness in our hospital.Immediate massaging of the globe and systemic therapy including acetylsalicylic acid, tinzaparin sodium and cortisone was initiated and hyaluronidase injections in the injection area were performed.In the further course, the patient developed necrotic and hemorrhagic skin and mucosal lesions, lagophthalmos, anterior and posterior segment ischemia and globe hypotonia with consecutive globe deformation.In the follow-up of 2.5 months, lid swelling, lagophthalmos and ptosis resolved and keratopathy improved but blindness, skin lesions and strabismus with reduced eye motility were still present and madarosis and early enophthalmos were detected.This case report illustrates fatal complications, their course, pathomechanism, management and outcome after hyaluronic acid filler injection in the glabella in a healthy woman.Case report: a 43-year-old caucasian female healthy patient underwent glabellar injection of 0.7 ml hyaluronic acid/ lidocaine (restylane) by a nonmedical practitioner.It was the patient's first filler injection, her former visual acuity was 20/20 on both eyes and no other diseases, including of the eyes, were present before the procedure.According to the patient, the visual field of her left eye already darkened during the procedure and massaging of the injection area with observation was performed, before she presented to our hospital 1 h later.One hour after the hyaluronic acid injection, the patient was treated with acetylsalicylic acid 100 mg (s.I.D, per oral), tinzaparin sodium 4.500 ie (s.I.D, subcutaneous), methylprednisolone 100 mg (s.I.D, intravenous for three days), then prednisone 90 mg per oral, pantoprazole 40 mg (s.I.D, per os, during steroid medication).Swelling of the left forehead and upper lid, ptosis and complete ophthalmoplegia were detectable.The left eye had no light perception, the intraocular pressure was normal, the left pupil barely reacted to light and showed a relative afferent pupillary defect.The anterior segment did not show further pathological findings.In the fundoscopy, the optic disc presented with sharp margins, the arteries were thinned, cherry red spot and retinal whitening were documented.Immediate massaging of the globe was attempted and further neurological diagnostic, including nuclear magnetic resonance imaging, was performed.Besides the ophthalmic pathologies, the neurological clinical findings were normal and in the medical imaging an ischemic optic neuropathy was suspected.Therapy with acetylsalicylic acid, tinzaparin sodium, methylprednisolone, pantoprazole, pain management and antiseptic compresses for the forehead was initiated.The dermatologists performed three hyaluronidase injections in the injection area.Two days after the glabellar hyaluronic acid injection, the periocular complications were still manifest with hemorrhagic changes on the upper lid.There was swelling, redness and surface irregularities on the left side of the forehead, nose and left upper lid and distinct ptosis.The left eye was slightly depressed while the right eye was slightly elevated indicating ophthalmoplegia.Two days after the hyaluronic acid injection, dexpanthenol 5% eye ointment (q.I.D.) and ofloxacin 3 mg/g eye ointment (q.I.D) were added to the patient's corrective therapy.The patient also developed skin lesions on the nose bridge, anterior segment ischemia and globe hypotonia.The conjunctiva was injected, the cornea had erosion, edema and descemet folds, the pupil was average sized, ovally warped, showing no light reaction.A perforation was ruled out.In the next two days, the skin on the forehead and the inner third of the upper lid showed early necrotic changes, the vertical lid fissure width was 9 mm, levator function 5 mm and a lagophthalmos of 3 mm was visible.Exophthalmometry was symmetrical and eye movement could be achieved approximately 5 degree downwards.The conjunctiva showed chemosis, keratopathy worsened and anterior chamber flattened to mid depth.A sonography revealed globe deformation and swelling of the choroidea.Due to the strong suspicion of an ophthalmic artery occlusion the otolaryngologists were involved in this case and found necrotic mucosal tissue at the top of the left middle nasal concha.The cranial nuclear magnetic resonance imaging was repeated, revealing a collapsed globe and edematous left optic nerve with diffusion restriction.In the angiography, an ophthalmic artery occlusion could not be confirmed or ruled out with certainty.Four days after the hyaluronic acid injection, the patient received an increased dose of dexpanthenol 5% eye ointment every 2 hour, and moisture chamber (during lagophthalmos), clindamycin 300 mg (q.I.D, per os, prescribed by dermatologists), nasal spray containing sea water and dexpanthenol were added to the patient's corrective therapy.The following 4 days (day 6 after hyaluronic acid injection), prednisolone 10 mg/ml eye drops (t.I.D) and atropine 0.5% eye drops (b.I.D) were added and prednisone was reduced to 60 mg (s.I.D, per os).Ten days after the injection complete lid closure could be achieved, depression, elevation and abduction improved slightly, corneal erosion decreased, no iridal ischemic signs were detected, the lens had little lentodonesis and the sonographic findings were constant.Two and a half weeks after the hyaluronic acid injection, lid swelling and ptosis resolved completely, showing a symmetrical lid fissure width of 10 mm and normal levator function.Amaurosis and severe globe hypotonia were still manifest.The conjunctiva was sparsely injected, the cornea was clear, stippled, without corneal erosion.Compared to the former medical findings, the anterior chamber deepened.The optic nerve was pale with indistinct margins, the retinal arteries were very thin and the retina was ischemic and edematous.No cherry red spot was visible and, in the sonography, the globe was still deformed.At day ten, the patient's corrective treatment with dexpanthenol 5% eye ointment was reduced to 6 times daily, prednisolone 10 mg/ml eye drops reduced (b.I.D), atropine 0.5% eye drops reduced (s.I.D) and prednisone reduced to 50 mg (s.I.D, per os).The prednisone dose was further reduced of 10 mg every three days, remaining on 10 mg) and clindamycin 300 mg was discontinued.Two and a half week after the injection, the patient's ofloxacin 3 mg/g eye ointment usage was reduced (t.I.D) and tinzaparin sodium 4.500 ie was discontinued.A further control examination after 6 weeks revealed redness and surface irregularity on the forehead and madarosis on the inner third of the upper lid.Abduction of 25 degree, complete elevation, depression of 15 degree and terminally restricted adduction with strabismus showing esotropia and hypertropia was visible.In the exophthalmometry a 2 mm more posterior location of the affected eye was detected.The visual acuity kept unchanged, the globe started to build up intraocular pressure, the anterior chamber further deepened, mild hyperemia of the iris was detectable, the pupil was still warped, developing posterior synechiae in the inferior nasal quadrant.The fundoscopy showed partially a slightly increased retinal vein caliber with tortuosity and very poor to no retinal artery filling with ischemic retinal areas.The oct revealed internal and external retinal atrophy with loss of retinal architecture.Six weeks after the hyaluronic acid injection, the prednisone dose was reduced to 5 mg (s.I.D, per os, for two weeks, then discontinued) and prednisolone 10 mg/ml eye drops frequency reduced (s.I.D).The patient discontinued the use of atropine 0.5% eye drops and ofloxacin 3 mg/ ml eye ointment.Two and a half month after the incident the clinical findings remained constant.Fundus of the left eye showed the optic nerve was pale with indistinct margins, very poor to no retinal artery filling, partially slightly increased retinal vein caliber, no cherry red spot and ischemic areas were detectable.At that point, the acetylsalicylic acid 100 mg was discontinued and prednisolone 10 mg/ml eye drops replaced with dexamethasone 1 mg/ml eye drops (s.I.D, without preservatives).Discussion: in our case, the injection of 0.7 ml of hyaluronic acid into the supratrochlear artery resulted in occlusion of the ophthalmic artery and its branches.The skin lesions were still present after 2.5 months.It was stated that ocular movement was weakened in every direction, which is in accordance with our patient's findings.In our patient normal levator function, completely recovered ptosis and better, but still reduced, eye movement and strabismus were present after 2.5 months.Further reported complications of ophthalmic artery occlusion were anterior segment ischemia, as was found in our patient, iris atrophy and phthisis bulbi on the long term.After 2.5 months, irregular widened pupil without iris atrophy or iris ischemia but mild hyperemia of the iris were obvious in our case.We found an early enophthalmos of the affected eye, which was also reported from another group after 6 months of follow-up.A phthisis bulbi or even enucleation in the further course cannot be excluded.Further known complications like brain infarcts or hemorrhage were ruled out in our patient.In our case, the immediate therapy consisted of acetylsalicylic acid, tinzaparin sodium, corticosteroids and observation.Regarding the lack of thrombotic cause of the occlusion, no intra-arterial thrombolysis was recommended.Due to extensive ischemic retinal and neuropathic changes already at time of presentation, the lack of benefit according to literature and to minimize further, possible complications, no hyaluronidase injections, except on the forehead, were performed since visual rehabilitation was not to be expected.In the angiography an ophthalmic artery occlusion could not be ascertained or ruled out.But the subsequent complications can be attributed to the branches of the ophthalmic artery, bearing in mind interindividual differences and anastomoses, and were also described in other studies as mentioned above.Further findings like the missing cherry rot spot due to retinal and choroidal insufficiency, extensive, whitish, edematous retinal ischemia, poor or no retinal artery filling and disc edema are seen in ophthalmic artery occlusion.Due to the restricted treatment possibilities and very poor outcome the further course remains to be seen.Conclusion: the outcome of ophthalmic artery occlusion following glabellar hyaluronic acid filler injection is very poor.It was essential that the practitioner has sufficient knowledge about facial anatomy, the implementation of this procedure and management of complications.The practitioner should be aware of potential devastating consequences and inform the patient specifically about this rare complication, since they might be irreversible and far-reaching.
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Event Description
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Nullification report for case (b)(4).This report was found to be a duplicate report to case (b)(4) on 25-apr-2022.Case (b)(4) will be nullified and all further reporting will be through case (b)(4).Case reference number (b)(4) is a literature report identified on 06-apr-2022 during literature search.This case refers to a 43-years-old caucasian female patient.This case was identified from the literature article davidova p, muller m, wenner y, konig c, kenikstul n, kohnen t.Ophthalmic artery occlusion after glabellar hyaluronic acid filler injection.American journal of ophthalmology case reports 2022;26:101407.Abstract: a healthy, 43-year-old woman underwent her first hyaluronic acid injection in the glabella and went blind on her left eye immediately thereafter.The massaging of the injection area and observation were performed, before she presented with swelling of the left forehead and upper lid, ptosis, complete ophthalmoplegia and blindness in our hospital.Immediate massaging of the globe and systemic therapy including acetylsalicylic acid, tinzaparin sodium and cortisone was initiated and hyaluronidase injections in the injection area were performed.In the further course, the patient developed necrotic and hemorrhagic skin and mucosal lesions, lagophthalmos, anterior and posterior segment ischemia and globe hypotonia with consecutive globe deformation.In the follow-up of 2.5 months, lid swelling, lagophthalmos and ptosis resolved and keratopathy improved but blindness, skin lesions and strabismus with reduced eye motility were still present and madarosis and early enophthalmos were detected.This case report illustrates fatal complications, their course, pathomechanism, management and outcome after hyaluronic acid filler injection in the glabella in a healthy woman.Case report: a 43-year-old caucasian female healthy patient underwent glabellar injection of 0.7 ml hyaluronic acid/ lidocaine (restylane) by a nonmedical practitioner.It was the patient's first filler injection, her former visual acuity was 20/20 on both eyes and no other diseases, including of the eyes, were present before the procedure.According to the patient, the visual field of her left eye already darkened during the procedure and massaging of the injection area with observation was performed, before she presented to our hospital 1 h later.One hour after the hyaluronic acid injection, the patient was treated with acetylsalicylic acid 100 mg (s.I.D, per oral), tinzaparin sodium 4.500 ie (s.I.D, subcutaneous), methylprednisolone 100 mg (s.I.D, intravenous for three days), then prednisone 90 mg per oral, pantoprazole 40 mg (s.I.D, per os, during steroid medication).Swelling of the left forehead and upper lid, ptosis and complete ophthalmoplegia were detectable.The left eye had no light perception, the intraocular pressure was normal, the left pupil barely reacted to light and showed a relative afferent pupillary defect.The anterior segment did not show further pathological findings.In the fundoscopy, the optic disc presented with sharp margins, the arteries were thinned, cherry red spot and retinal whitening were documented.Immediate massaging of the globe was attempted and further neurological diagnostic, including nuclear magnetic resonance imaging, was performed.Besides the ophthalmic pathologies, the neurological clinical findings were normal and in the medical imaging an ischemic optic neuropathy was suspected.Therapy with acetylsalicylic acid, tinzaparin sodium, methylprednisolone, pantoprazole, pain management and antiseptic compresses for the forehead was initiated.The dermatologists performed three hyaluronidase injections in the injection area.Two days after the glabellar hyaluronic acid injection, the periocular complications were still manifest with hemorrhagic changes on the upper lid.There was swelling, redness and surface irregularities on the left side of the forehead, nose and left upper lid and distinct ptosis.The left eye was slightly depressed while the right eye was slightly elevated indicating opthalmoplegia.Two days after the hyaluronic acid injection, dexpanthenol 5% eye ointment (q.I.D.) and ofloxacin 3mg/g eye ointment (q.I.D) were added to the patient's corrective therapy.The patient also developed skin lesions on the nose bridge, anterior segment ischemia and globe hypotonia.The conjunctiva was injected, the cornea had erosion, edema and descemet folds, the pupil was average sized, ovally warped, showing no light reaction.A perforation was ruled out.In the next two days, the skin on the forehead and the inner third of the upper lid showed early necrotic changes, the vertical lid fissure width was 9 mm, levator function 5 mm and a lagophthalmos of 3 mm was visible.Exophthalmometry was symmetrical and eye movement could be achieved approximately 5 degree downwards.The conjunctiva showed chemosis, keratopathy worsened and anterior chamber flattened to mid depth.A sonography revealed globe deformation and swelling of the choroidea.Due to the strong suspicion of an ophthalmic artery occlusion the otolaryngologists were involved in this case and found necrotic mucosal tissue at the top of the left middle nasal concha.The cranial nuclear magnetic resonance imaging was repeated, revealing a collapsed globe and edematous left optic nerve with diffusion restriction.In the angiography, an ophthalmic artery occlusion could not be confirmed or ruled out with certainty.Four days after the hyaluronic acid injection, the patient received an increased dose of dexpanthenol 5% eye ointment every 2 hour, and moisture chamber (during lagophthalmos), clindamycin 300 mg (q.I.D, per os, prescribed by dermatologists), nasal spray containing sea water and dexpanthenol were added to the patient's corrective therapy.The following 4 days (day 6 after hyaluronic acid injection), prednisolone 10 mg/ml eye drops (t.I.D) and atropine 0.5% eye drops (b.I.D) were added and prednisone was reduced to 60 mg (s.I.D, per os).Ten days after the injection complete lid closure could be achieved, depression, elevation and abduction improved slightly, corneal erosion decreased, no iridal ischemic signs were detected, the lens had little lentodonesis and the sonographic findings were constant.Two and a half weeks after the hyaluronic acid injection, lid swelling and ptosis resolved completely, showing a symmetrical lid fissure width of 10 mm and normal levator function.Amaurosis and severe globe hypotonia were still manifest.The conjunctiva was sparsely injected, the cornea was clear, stippled, without corneal erosion.Compared to the former medical findings, the anterior chamber deepened.The optic nerve was pale with indistinct margins, the retinal arteries were very thin and the retina was ischemic and edematous.No cherry red spot was visible and, in the sonography, the globe was still deformed.At day ten, the patient's corrective treatment with dexpanthenol 5% eye ointment was reduced to 6 times daily, prednisolone 10 mg/ml eye drops reduced (b.I.D), atropine 0.5% eye drops reduced (s.I.D) and prednisone reduced to 50 mg (s.I.D, per os).The prednisone dose was further reduced of 10 mg every three days, remaining on 10 mg) and clindamycin 300 mg was discontinued.Two and a half week after the injection, the patient's ofloxacin 3mg/g eye ointment usage was reduced (t.I.D) and tinzaparin sodium 4.500 ie was discontinued.A further control examination after 6 weeks revealed redness and surface irregularity on the forehead and madarosis on the inner third of the upper lid.Abduction of 25 degree, complete elevation, depression of 15 degree and terminally restricted adduction with strabismus showing esotropia and hypertropia was visible.In the exophthalmometry a 2 mm more posterior location of the affected eye was detected.The visual acuity kept unchanged, the globe started to build up intraocular pressure, the anterior chamber further deepened, mild hyperemia of the iris was detectable, the pupil was still warped, developing posterior synechiae in the inferior nasal quadrant.The fundoscopy showed partially a slightly increased retinal vein caliber with tortuosity and very poor to no retinal artery filling with ischemic retinal areas.The oct revealed internal and external retinal atrophy with loss of retinal architecture.Six weeks after the hyaluronic acid injection, the prednisone dose was reduced to 5 mg (s.I.D, per os, for two weeks, then discontinued) and prednisolone 10 mg/ml eye drops frequency reduced (s.I.D).The patient discontinued the use of atropine 0.5% eye drops and ofloxacin 3 mg/ ml eye ointment.Two and a half month after the incident the clinical findings remained constant.Fundus of the left eye showed the optic nerve was pale with indistinct margins, very poor to no retinal artery filling, partially slightly increased retinal vein caliber, no cherry red spot and ischemic areas were detectable.At that point, the acetylsalicylic acid 100 mg was discontinued and prednisolone 10 mg/ml eye drops replaced with dexamethasone 1 mg/ml eye drops (s.I.D, without preservatives).Discussion: in our case, the injection of 0.7 ml of hyaluronic acid into the supratrochlear artery resulted in occlusion of the ophthalmic artery and its branches.The skin lesions were still present after 2.5 months.It was stated that ocular movement was weakened in every direction, which is in accordance with our patient's findings.In our patient normal levator function, completely recovered ptosis and better, but still reduced, eye movement and strabismus were present after 2.5 months.Further reported complications of ophthalmic artery occlusion were anterior segment ischemia, as was found in our patient, iris atrophy and phthisis bulbi on the long term.After 2.5 months, irregular widened pupil without iris atrophy or iris ischemia but mild hyperemia of the iris were obvious in our case.We found an early enophthalmos of the affected eye, which was also reported from another group after 6 months of follow-up.A phthisis bulbi or even enucleation in the further course cannot be excluded.Further known complications like brain infarcts or hemorrhage were ruled out in our patient.In our case, the immediate therapy consisted of acetylsalicylic acid, tinzaparin sodium, corticosteroids and observation.Regarding the lack of thrombotic cause of the occlusion, no intra-arterial thrombolysis was recommended.Due to extensive ischemic retinal and neuropathic changes already at time of presentation, the lack of benefit according to literature and to minimize further, possible complications, no hyaluronidase injections, except on the forehead, were performed since visual rehabilitation was not to be expected.In the angiography an ophthalmic artery occlusion could not be ascertained or ruled out.But the subsequent complications can be attributed to the branches of the ophthalmic artery, bearing in mind interindividual differences and anastomoses, and were also described in other studies as mentioned above.Further findings like the missing cherry rot spot due to retinal and choroidal insufficiency, extensive, whiteish, edematous retinal ischemia, poor or no retinal artery filling and disc edema are seen in ophthalmic artery occlusion.Due to the restricted treatment possibilities and very poor outcome the further course remains to be seen.Conclusion: the outcome of ophthalmic artery occlusion following glabellar hyaluronic acid filler injection is very poor.It was essential that the practitioner has sufficient knowledge about facial anatomy, the implementation of this procedure and management of complications.The practitioner should be aware of potential devastating consequences and inform the patient specifically about this rare complication, since they might be irreversible and far-reaching.
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Manufacturer Narrative
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Company comment: nullification report for case (b)(4).Found to be a duplicate to case (b)(4).The serious events of blindness unilateral, ophthalmic artery occlusion, ophthalmoplegia, optic ischaemic neuropathy, anterior segment ischaemia, retinal ischaemia and implant site necrosis were considered expected and possibly related to the treatment.Seriousness criteria included the need for multiple medical interventions and permanent damage.The non-serious, expected events of erythema, swelling and haemorrhage at implant site, cutaneous contour deformity, eyelid ptosis, enophthalmos, strabismus, papilloedema, corneal oedema, conjunctival oedema, retinal oedema, choroidal effusion and the unexpected events of lagophthalmos, madarosis, hypotony of eye, corneal erosion, pupillary reflex impaired, conjunctival hyperaemia, iris atrophy, atrophy of globe, retinal degeneration and vitreous detachment were considered possibly related to the treatment.Iris atrophy, atrophy of globe, retinal degeneration and vitreous detachment were considered to be secondary events of the ophthalmic artery occlusion.The potential root cause include intravascular filler injection leading to vascular occlusion and its manifestations.Potential contributory factors include injection technique and treatment performed by a non-medical practitioner.The case meets the criteria for expedited reporting to the regulatory authorities.Final manufaturer comment: routine investigations have been performed and provide sufficient information to assess the potential root cause and indicate a possible association to the treatment procedure.Lot number was not reported and the product could not be verified.The information in this case does not indicate a non-conforming product or malfunction.The performed investigations are therefore considered adequate and no additional investigations will be conducted.Capa comment: no corrective or preventive actions are deemed necessary based on the outcome of the performed investigations.
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