ABSTRACT
BACKGROUND: Müller's muscle-conjunctival resection surgery presumably works by advancing the levator aponeurosis of the upper eyelid. The amount of blepharoptosis and the lid's response to the instillation of phenylephrine hydrochloride onto the superior ocular fornix are used to determine the extent of surgery needed. OBJECTIVES: To demonstrate the procedure developed and popularized by Allen M. Putterman, MD, performed by Michael Mercandetti, MD, MBA, and to describe the relationship between the amount of Müller's muscle-conjunctival resection performed and the amount of elevation achieved. METHODS: Data were retrospectively analyzed based on surgical cases done over a 5-year period by one surgeon (A.M.P.). RESULTS: A linear regression model was developed. From this regression a simple table correlating the amount of resection with the amount of elevation desired was derived. CONCLUSION: The surgeon will need to modify the table based on his or her clinical experience and postoperative results.
Subject(s)
Blepharoplasty/methods , Blepharoptosis/surgery , Conjunctiva/surgery , Eyelids/surgery , Muscle, Smooth/surgery , Oculomotor Muscles/surgery , Phenylephrine , Adolescent , Adult , Aged , Aged, 80 and over , Blepharoplasty/adverse effects , Female , Humans , Male , Middle Aged , Muscle Contraction/drug effects , Muscle, Smooth/drug effects , Muscle, Smooth/innervation , Retrospective StudiesABSTRACT
One of the earliest histopathological signs of diabetic retinopathy is a selective loss of intramural pericytes from retinal capillaries. In the present study, the retinal vessels of rats with streptozotocin-induced diabetes (STZ Wistar) and rats with genetically-induced insulin dependent diabetes mellitus (BB Wistar) and non-insulin dependent diabetes mellitus (SHR/N-corpulent) were examined after 6 to 8 months duration for diabetes-related retinal microangiopathies. The SHR/N-corpulent (cp) rats were fed a 54% sucrose diet, whereas the STZ Wistar and BB Wistar rats were fed laboratory chow for 32 to 36 weeks. In all the diabetic rats, the retinal capillaries in enzyme-digested flat mounts exhibited an increase in periodic-acid-Schiff (PAS) staining and loss of pericytes compared to their respective euglycemic controls. Pericyte "ghosts", like those defined in human diabetes as intramural pockets lacking normal cell contents, were documented by high resolution micrographs in all the diabetic rats. Endothelial cell proliferation, capillary dilation, and varicose loop formation were noted in some of the diabetic rats. Hence, similar capillary lesions were found in very different groups of diabetic rats. The findings suggest that a chronic high tissue concentration of glucose is the underlying factor which triggers pathogenesis in the pericyte. Hyperglycemia-induced activation of endogenous aldose reductase of the polyol pathway is probably the initial insult, but other factors such as advanced glycosylation products may affect the final outcome.
