Arterial Wall and Tissue Penetration Force With Various Cannulas and Needles.

BACKGROUND: Vascular penetration during aesthetic filler injections can cause serious side effects such as skin necrosis and blindness. OBJECTIVES: The objective of this study was to analyze the effect of cannula brand and gauge on the risk of vascular penetration. METHODS: The minimal force to penetrate the superficial temporal artery with 3 cannula brands and 1 needle brand in 4 sizes (22, 25, 27, and 30 gauge) was measured in 4 fresh frozen cadavers utilizing a force gauge that measured as low as 0.1 Newtons. Tissue penetration force in the subdermal plane of the nasolabial fold was measured and compared with retrospective training data in live humans. The arterial penetration test was repeated at a second site on 1 fresh cadaver with 2 different force gauges. RESULTS: Significantly lower forces were needed with all size needles vs the same gauge cannulas in all brands to penetrate the cadaveric artery and advance in the subdermal plane of the nasolabial fold in both cadavers and live humans. To successfully enter the artery in a cadaver with any cannula, numerous attempts were necessary. The tissue penetration force in the subdermal plane of the nasolabial fold in a cadaver was not significantly different than in a living person; however, it was significantly higher than the arterial penetration force in a dissected cadaver. CONCLUSIONS: All gauge cannulas (including 27 and 30 gauge), require more force than the same size needle to penetrate an artery. However, it appears that friction coefficient and flexibility, not the arterial penetration force, are the most important factors in keeping the instrument outside the vessel.

Focused ultrasound stimulation on meibomian glands for the treatment of evaporative dry eye.

Current treatments for meibomian gland dysfunction have several limitations, creating a necessity for other advanced treatment options. The purpose of this study is to determine the effectiveness of focused ultrasound stimulation for the treatment of dry eye disease caused by meibomian gland dysfunction. An in vivo study of nine Dutch Belted rabbits was conducted with focused ultrasound stimulation of the meibomian glands. A customized line-focused ultrasonic transducer was designed for treatment. Fluorescein imaging, Schirmer's test, and Lipiview II ocular interferometer were used to quantify outcomes from three aspects: safety, tear production, and lipid layer thickness. Both tear secretion and lipid layer thickness improved following ultrasound treatment. Five to 10 min after the ultrasound treatment, the mean values of lipid layer thickness increased from 55.33 ± 11.15 nm to 95.67 ± 22.77 nm (p < 0.05), while the mean values measured with the Schirmer's test increased from 2.0 ± 2.3 to 7.2 ± 4.3 (p < 0.05). Positive effects lasted more than three weeks. Adverse events such as redness, swelling, and mild burn, occurred in two rabbits in preliminary experiments when the eyelids sustained a temperature higher than 42°C. No serious adverse events were found. The results suggest that ultrasound stimulation of meibomian glands can improve both tear production and lipid secretion. Ultimately, ultrasound stimulation has the potential to be an option for the treatment of evaporative dry eye disease caused by meibomian gland dysfunction.

Thyroid eye disease with choroidal folds.

Purpose: To determine the clinical course of patients with chorioretinal folds (CRF) in thyroid eye disease (TED).Methods: A multi-center retrospective case series of patients with TED who developed CRF.Results: Ten patients (17 eyes) with CRF related to TED were identified. The mean age of presentation was 59.3 ± 8.3 years old. The majority of patients were male (70%), hyperthyroid (70%), hyperopic (53%), had a history of radioactive iodine (60%), and currently on methimazole treatment (30%). Three patients (3 eyes) had unilateral involvement of CRF with bilateral TED. The average clinical activity score was 3.6 ± 2.1 at the time of presentation. The most commonly enlarged extraocular muscles were medial (76%), inferior (64%), superior (64%) and lateral rectus (35%). Compressive optic neuropathy was seen in 47% of eyes. Treatment included oral prednisone (70%), orbital decompression (59%), thyroidectomy (20%) and tocilizumab (10%). The CRF did not resolve over a follow up period of 24.7 ± 23.7 months in 70% of eyes. There was no significant difference in average axial length (25.7 ± 4.9 mm) and optic nerve to optic strut distance (37.8 ± 3.9 mm) between patients with CRF and the eight age-and sex-matched TED control patients without CRF (p = 0.81 and 0.65 respectively). A univariable and multivariable analysis found an enlarged inferior rectus as a factor in TED patients with persistent CRF.Conclusions: CRF are often an indicator of visually threatening situations and often do not resolve despite treatment of TED.

Minimally invasive options for the brow and upper lid.

Eyebrow and upper eyelid aging occurs in all tissue planes, and manifests most commonly in skin quality, tissue volume loss (soft tissue and bone), and tissue descent. All these involutional changes are amenable to less-invasive (nonsurgical) interventions with natural and aesthetically pleasing results. It is critical for aesthetic facial surgeons to familiarize themselves with these procedures because they are in high demand by patients. This article outlines current concepts of nonsurgical management options for brow and upper eyelid aging. The anatomy and age-related changes in these structures are reviewed, and minimally invasive techniques to address these changes are detailed.

Minimally invasive surgical adjuncts to upper blepharoplasty.

A variety of surgical adjuncts can be added to upper eyelid blepharoplasty with the goal of enhancing surgical results and patient satisfaction. All of these procedures are minimally invasive and most are performed through a standard eyelid crease incision. These procedures can be added to stabilize or conservatively lift the outer brow, prevent the stigmata of postoperative volume loss, improve the brow-eyelid transition and contour, and reposition a prolapsed lacrimal gland. The procedures are generally straightforward, easily learned, and complication free. Familiarity with these techniques provides the aesthetic eyelid surgeon with added options to improve surgical results.

Evolving Minimally Invasive Techniques for Tear Trough Enhancement.

PURPOSE: The aim of this study is to investigate whether volumetric enhancement of the infraorbital rim area or, alternatively, of the deep medial cheek, results in greater improvement of tear trough deformity. METHODS: This prospective, single-blind study recruited 12 patients seeking correction of tear trough deformity. Pretreatment standardized photographs were obtained after which patients were randomized to receive hyaluronic acid gel filler augmentation of the tear trough on one side and hyaluronic acid gel augmentation of the cheek on the contralateral side. The patients were then re-examined at 3 weeks postinjection when standardized photographs were taken again. Following the photographs, filler was added to the side and location where they were not used at the original treatment, resulting in added volume in both the cheek and the tear trough. The patients returned 3 weeks later when final photographs were taken. The pre- and post-treatment images were randomized and evaluated by 3 masked observers asked to evaluate the depth of tear trough. RESULTS: There was a significant improvement in the depth of the tear trough rating after initial treatment on the side treated in the tear trough (p = 0.0001). There was not a significant change in depth of tear trough rating, however, on the side receiving cheek only treatment (p = 0.0963). There was a statistically significant change in tear trough rating after both tear trough and cheek had been treated on each side (p = 0.001). There was no statistically significant difference between sides after lid and cheek treatment had been completed on each side (p = 0.5986). Intraclass correlation between reviewers for all subjects was excellent at 0.94. Tear trough injections were more technique sensitive than cheek volume augmentation to achieve satisfactory results. There were no complications from cheek volume enhancement. Varying degrees of ecchymosis were encountered with tear trough injections. CONCLUSIONS: When the patient's primary concern is the appearance of the tear trough, and the physician is limited to treating either the tear trough or the cheek alone, it appears that treatment in the tear trough offers greater improvement in the appearance of the tear trough deformity when compared with treatment in the cheek alone.

Characterization and outcomes of repeat orbital decompression for thyroid-associated orbitopathy.

Orbital decompression for thyroid-associated orbitopathy (TAO) is commonly performed for disfiguring proptosis, congestion, and optic neuropathy. Although one decompression typically achieves goals, a small percentage requires repeat decompression. We performed a 10-year retrospective chart review of all orbital decompressions for TAO at a single tertiary referral institution. Four-hundred and ninety-five orbits (330 patients) were decompressed for TAO, with 45 orbits (37 patients) requiring repeat decompression. We reviewed the repeat cases for indications, clinical activity scores, approach, walls decompressed, and outcomes. Nine percent of orbits required repeat decompression for proptosis (70%), optic neuropathy (25%) or congestion (45%). Sixty-four percent were for recurrence of disease, 36% were for suboptimal decompression. Three incisional approaches were used: lateral upper eyelid crease, inferior transconjunctival, and transcaruncular, with inferior transconjunctival being most common. Of the three walls removed, deep lateral, inferior, and medial, the deep lateral wall was most common (51%). A repeat lateral decompression was the most frequent pattern. Of 37 patients requiring repeat decompression, 40% had diplopia prior to repeat, and an additional 24% developed diplopia after the repeat. Whereas previous studies published by our group cited only 2.6% of deep lateral wall orbital decompressions leading to new-onset primary gaze diplopia, repeat orbital decompressions have a much higher rate of post-operative diplopia. The new onset primary gaze diplopia after repeat decompression group had a higher average preoperative CAS (3.3 vs. 2.4, p < 0.01), higher mean blood loss (56 vs. 19 mL, p = 0.04), more frequent medial wall decompressions (47% vs. 29%, p = 0.33), and greater proptosis reduction (2.4 vs. 1.7 mm, p = 0.24).

Late central visual recovery after traumatic globe displacement into the maxillary sinus.

Globe prolapse into the maxillary sinus after trauma is rare and usually portends a very poor visual prognosis. The authors present an unusual case of late restoration of central vision after such trauma. A 20-year-old man presented after motorcycle injury with a large right floor and medial orbital wall fracture with displacement of the globe into the maxillary sinus. The patient had no light perception on initial exam and was emergently taken to the operating room for globe exploration. No globe rupture was found, and the right orbital floor and medial wall fractures were repaired. Three days of intravenous methylprednisolone at 250 mg every 6 hours was administered postoperatively with no change in visual status, and the patient was discharged home on a rapid oral prednisone taper. At postoperative week 6, vision had returned to 20/20 OD centrally. Visual field testing revealed a central tunnel of vision. The patient's visual function continues to remain stable 2 years after the initial trauma.

Antibody-mediated clearance of amyloid-beta peptide from cerebral amyloid angiopathy revealed by quantitative in vivo imaging.

Cerebral amyloid angiopathy (CAA) is the accumulation of amyloid-beta peptide (Abeta) in the vessel wall of arteries in the brain. Because CAA is commonly associated with Alzheimer's disease (AD), characterized by parenchymal deposition of the same peptide in the form of senile plaques, there is considerable interest in the relationship of the two deposits in generating human disease. The study of CAA is of particular importance for immunotherapeutic approaches to AD, because reports of anti-Abeta immunotherapy in mice and humans have suggested that, whereas CAA appeared resistant to clearance, its response to this treatment promoted potential adverse effects, including meningoencephalitis. We used multiphoton microscopy and longitudinal imaging to monitor CAA in a mouse model of amyloid deposition to evaluate the effects of anti-Abeta passive immunotherapy. We found detectable clearance of CAA deposits within 1 week after a single administration of antibody directly to the brain, an effect that was short-lived. Chronic administration of antibody over 2 weeks led to more robust clearance without evidence of hemorrhage or other destructive changes. We found that the progressive clearance of Abeta from vessels follows distinct kinetics from what has been previously reported for clearance of plaques (parenchymal deposits of Abeta). This quantitative in vivo imaging approach directly demonstrates that CAA in a transgenic mouse model can be cleared with an optimized immunotherapy.

Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease.

Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the beta-amyloid as senile plaques and cerebral amyloid angiopathy. We have characterized the natural history of beta-amyloid deposition in APPswe/PS1dE9 mice, a particularly aggressive transgenic mouse model generated with mutant transgenes for APP (APPswe: KM594/5NL) and PS1 (dE9: deletion of exon 9). Ex vivo histochemistry showed Abeta deposition by 4 months with a progressive increase in plaque number up to 12 months and a similar increase of Abeta levels. In vivo multiphoton microscopy at weekly intervals showed increasing beta-amyloid deposition as CAA and plaques. Although first appearing at an early age, CAA progressed at a significantly slower rate than in the Tg2576 mice. The consistent and early onset of beta-amyloid accumulation in the APPswe/PS1dE9 model confirms its utility for studies of biochemical and pathological mechanisms underlying beta-amyloid deposition, as well as exploring new therapeutic treatments.

The cerebral beta-amyloid angiopathies: hereditary and sporadic.

We review the clinical, radiologic, and neuropathologic features of the hereditary and sporadic forms of cerebral amyloid angiopathy (CAA) associated with vascular deposition of the beta-amyloid peptide. Amino acid substitutions at 4 sites in the beta-amyloid precursor protein, all situated within the beta-amyloid peptide sequence itself, have been shown to cause heritable forms of CAA. The vascular diseases caused by these mutations are associated primarily with cerebral hemorrhages, white matter lesions, and cognitive impairment, and only variable extents of the plaque and neurofibrillary pathologies characteristic of Alzheimer disease. Sporadic CAA typically presents 20 or more years later than hereditary CAA, but is otherwise characterized by a comparable constellation of recurrent cerebral hemorrhages, white matter lesions, and cognitive impairment. The clinical, radiologic and pathologic similarities between hereditary and sporadic CAA suggest that important lessons for this common age-related process can be learned from the mechanisms by which mutation makes beta-amyloid tropic or toxic to vessels.