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 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The complications of blepharoplasty are infrequent, most often minor and transient, and rarely major and permanent with functional or aesthetic consequences. Treatment is above all preventive with screening of "at risk" patients in whom blepharoplasty would be contra-indicated. Patients must be informed of possible risks through informative booklets stressing the most important points. The complications may affect vision. Partial or complete visual loss due to ischemic optic neuropathy, or rarely to compression of the ocular globe by intraorbital hemorrhage, is the most serious complication. Other visual complications include oculomotor disorders, keratoconjunctivitis sicca, epiphora, and chemosis of lymphatic origin. Eyelid complications are more frequent: ptosis of the upper eyelid or lagophthalmia caused by incorrect resection of the skin, scarring, and eyelid fold anomalies. The most severe aesthetic complication is the malposition of the lower eyelid resulting in retraction, lagophthalmia, ectropion, deformation of the external canthus, or lower eyelid tissue relaxation. These malpositions are often minor, sometimes reversible, but they can be major, with psychological, aesthetic, and functional consequences. Other local complications include enophthalmia and hypo- or hypercorrection. General complications may include pigmentation anomalies or infections extending as far as the orbital fat tissue. Finally, complications observed after the newer procedures of laser surgery include ectropion, burns and residual redness. Complications related to periocular injections of filling material are also mentioned. The discussion of these complications is followed by a comprehensive review of the prevention, diagnosis and management of the complications after blepharoplasty.
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PMID:Complications of blepharoplasty. 1718 5

Spontaneous dissection of the cervical internal carotid artery (sICAD) causes, in more than 90% of patients, carotid territory ischemia, local signs and symptoms on the side of dissection, or both, whereas the remaining sICAD remain clinically asymptomatic. Local signs and symptoms include head, facial, or neck pain, Horner syndrome, pulsatile tinnitus, and cranial nerve palsy. Head, facial, or neck pain occurs in 64-74% and is the presenting symptom in up to 58.5%, and the only manifestation in 2.2-4.5%. Headache is observed in 65-68%, facial pain in 34-53%, and neck pain in 9-26%. Horner syndrome consisting essentially of miosis and ptosis is detected in 28-41%. Cranial nerve palsy is reported in 8-16%; the lower cranial nerves IX-XII are most commonly affected, in particular the hypoglossal nerve. The facial nerve may also be involved; dysgeusia results mainly from involvement of the chorda tympani (0.5-7.0%) or the glossopharyngeal nerve. Transient pareses of the ocular motor (III, IV and VI) and trigeminal nerves have been observed. Pulsatile tinnitus is reported in 16-27%. About three quarters of sICAD cause ischemic events, which include ischemic stroke in 80-84%, transient ischemic attack in 15-16%, amaurosis fugax in 3%, ischemic optic neuropathy in 4%, and retinal infarct in 1%. Patients with sICAD causing ischemia show a lower prevalence of Horner syndrome and palsy of the caudal cranial nerves than patients with sICAD causing no ischemic events, whereas headache, neck pain, and pulsatile tinnitus are equally frequent in both groups. After an ischemic stroke, independency defined by a moderate Rankin scale score of 0-2 occurs in 63-90%, whereas the outcome of retinal infarct and ischemic optic neuropathy are not well known.
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PMID:Clinical manifestations of carotid dissection. 1729 Jan 13

A 71-year-old woman was admitted with fever, headache, and weight loss associated with elevated inflammatory markers. She developed acute bilateral ophthalmoplegia and asymmetrical ptosis, rapidly followed by anterior ischemic optic neuropathy. Although the first temporal artery biopsy was negative, contralateral temporal artery biopsy revealed features consistent with giant cell arteritis. Even while under steroid therapy, she died a few days later from myocardial infarction. Acute bilateral complete ophthalmoplegia is a rare presentation of a limited number of possible diseases. Among these, giant cell arteritis should be suspected in the appropriate clinical scenario.
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PMID:Tempo(ral) was the heart of the matter. 2902 75