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Device Problem Adverse Event Without Identified Device or Use Problem (2993)
Patient Problems Embolism (1829); Nausea (1970); Loss of Vision (2139); Ptosis (2620); No Code Available (3191)
Event Type  Injury  
Manufacturer Narrative
Lot number was not reported. Capa comment: the information in this single case does not suggest involvement of a nonconforming product or quality problem and will not initiate a corrective or preventive action. This case was received late by the pv department and is included in the investigation of (b)(4). Pharmacovigilance comment: the serious expected event of blindness unilateral and eye infarction were considered possibly related to the treatment. Serious criteria included permanent damage or disability. The non-serious unexpected events of retinal ischaemia, eyelid ptosis, nausea, mydriasis, enophthalmos, optic nerve disorder, ophthalmoplegia, conjunctival oedema, corneal defect, corneal oedema, retinal haemorrhage, maculopathy, papilloedema and embolism were considered possibly related to the treatment. Potential etiologies include emboli and ischemia associated with intravascular injection. Potential contributory factors include injection technique and vascular variation associated with previous rhinoplasty. The case meets the criteria for expedited reporting to the regulatory authorities.
Event Description
Case reference number (b)(4) is a spontaneous report received on 03-jun-2017 from a physician concerning a (b)(6) year-old male patient. This case has been published in the literature: roberts sa, arthurs bp. Severe visual loss and orbital infarction following periorbital aesthetic poly-(l)-lactic acid (plla) injection. Ophthalmic plast reconstr surg. 2012 may-jun;28(3):e68-70. A (b)(6) year-old male was referred reporting physician's department from the emergency room the day after receiving a treatment in the lateral nasal and periorbital areas of the face with plla subcutaneous filler (sculptra). The patient described a sharp pain behind his left eye immediately following an injection in the left periorbital region followed by a sustained, deep boring pain. Concurrent with the onset of pain, he noticed a sudden and profound ipsilateral loss of vision. He was counseled by his treating physician that some pain may be expected as a side effect of treatment and that the visual changes would be transient. The patient continued to have an intense pain throughout the night, with minimal relief from acetaminophen and ibuprofen. As this was his second of 6 planned injection treatments to restore volume to his periorbital regions, in particular his medial canthal and lower eyelid area, he worried about the differences between this current injection and the previous. The following morning, he presented to the hospital out of concern for his persistent loss of vision in the left eye and the now slowly subsiding pain. He also experienced nausea and reported an inability to open or move his left eye. His medical history was significant for a previous rhinoplasty, (b)(6) of 10 years duration, and (b)(6) related lipodystrophy for which he was being treated with plla subcutaneous filler. His past ocular history was significant only for mild-to-moderate myopia corrected via spectacles, and he denied any known drug allergies. His medications included (b)(6) and 2 other (b)(6) medications as part of his highly active (b)(6) therapy regimen. On examination, his best corrected visual acuity was 20/20 in the right eye and light perception with projection in the left eye. The patient had an approximate 4-mm ptosis of the left upper eyelid. He also had a fixed and irregularly dilated left pupil measuring 6. 5 mm. The intraocular pressure was 10 mm hg in the right eye and registered 0 - 1 mm hg in the left eye. Exophthalmometry measurements indicated a small, relative left enophthalmos of 1 mm. On extraocular movement testing, right eye ductions were full and complete; however, there was a near total ophthalmoplegia of the left eye with some residual but minimal supra- and infraduction. Slit-lamp examination was unremarkable for the right eye. Examination of the left eye revealed inferior conjunctival chemosis, a paracentral epithelial defect of the cornea, stromal corneal edema with descemet membrane folds, and a deep and formed anterior chamber with a moderate 2 - 3+ cellular reaction plus pigment (corneal epithelial defect and descemet membrane folds of left eye 3 days after injury. The left upper eyelid is manually retracted, masking the ptosis. Note the conjunctival chemosis temporally). Posterior segment examination was normal in the right eye (normal, posterior pole fundus photograph of unaffected fellow eye). There was no vitritis on left eye examination, but the retina demonstrated inner retinal hemorrhages, venous dilatation, macular pallor, and arteriolar narrowing (macular pallor, venous dilatation, mild arteriolar narrowing, and a large inner retinal hemorrhage of the left eye 3 days after injury. The fundus photograph clarity was limited by coexistent corneal edema). The patient also had a mild optic disc edema on the affected side. There were no entrance or exit wounds noted over the surface of the globe, anteriorly or posteriorly. A ct scan was performed to assess the posterior globe and orbital structures, but the study did not reveal any additional information and was reported as normal. Complete blood count, electrolytes, and a coagulation profile were all unremarkable. Fundus fluorescein angiography was performed 2 days later and was significant for profoundly limited and delayed choroidal, arterial, and venous filling. Angiography and further history suggested an embolic orbital infarction as the mechanism of injury. The patient was lost to follow-up after his initial visits and elected to continue his medical care at another center. By personal communication, he reported that his ocular movements and ptosis of the left eye improved, but his vision remained depressed. It was interesting to note that the patient in this case also experienced a ptosis and ophthalmoplegia coupled with his visual loss. The ptosis and ophthalmoplegia improved with time (as reported by the patient), and the more sensitive retinal and neural tissue of the eye remained affected. Another likely risk factor for the patient was his previous history of rhinoplasty, which may have compromised some of these anastomoses, rendering an additional susceptibility to ischemia.
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Manufacturer (Section D)
seminariegatan 21
uppsala, SE-75 2 28
SW SE-752 28
Manufacturer (Section G)
seminariegatan 21
uppsala, SE-75 2 28
SW SE-752 28
Manufacturer Contact
randy russell
14501 n. freeway
fort worth, TX 76177
MDR Report Key9707952
MDR Text Key192435441
Report Number9710154-2020-00027
Device Sequence Number1
Product Code LMH
Combination Product (y/n)N
Reporter Country CodeCA
PMA/PMN Number
Number of Events Reported1
Summary Report (Y/N)N
Report Source Manufacturer
Source Type foreign,health professional,l
Reporter Occupation
Type of Report Initial
Report Date 02/13/2020
1 Device was Involved in the Event
1 Patient was Involved in the Event
Date FDA Received02/13/2020
Is this an Adverse Event Report? Yes
Is this a Product Problem Report? No
Device Operator
Was Device Available for Evaluation? No
Is the Reporter a Health Professional? Yes
Was the Report Sent to FDA?
Event Location No Information
Date Manufacturer Received06/03/2017
Was Device Evaluated by Manufacturer? No
Is the Device Single Use? Yes
Is This a Reprocessed and Reused Single-Use Device? No
Type of Device Usage Unkown

Patient Treatment Data
Date Received: 02/13/2020 Patient Sequence Number: 1