CHIN IMPLANT DALLAS AFTER CARE TUTORIAL
DALLAS FACIAL PLASTIC SURGEON, DR. SAMUEL LAM, DISCUSSES THE AFTER CARE FOLLOWING CHIN AUGMENTATION USING EXTENDED ANATOMIC CHIN IMPLANTS.
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Goldenhar Syndrome
History
The first observations of the Goldenhar-like features were first reported by Von Arlt in 1881.
Goldenhar, in 1952, collected and classified these findings and described the Goldenhar syndrome.
The syndrome was consisting of preauricular appendages and fistula, and epibulbar dermoids.
Gorlin, in 1963, introduced the term Oculoauriculovertebral (OAV) dysplasia to describe patients with unilateral microtia, macrostomia, mandibular hypoplasia, vertebral anomalies, and epibulbar dermoids.
Hollowich and Verbeck in 1969 described a patient with Goldenhar’s syndrome and reviewed 33 other cases reported since the Goldenhar’s original article.
The clinical manifestations of Goldenhar syndrome closely resemble those of hemifacial microsomia ( first and second brachial arch syndrome).
Smith, in 1978, used the term facio-auriculo-vertebral-anomalad to include both Goldenhar syndrome and hemifacial microsomia.
Incidence and Prevalence
Goldenhar’s syndrome is rare .
The true incidence is unknown, and since there are other syndromes with similar features, there is still confusion over which cases should be classified specifically as Goldenhar’s syndrome.
In Goldenhar patient, the clinical findings classically include the following triad :- 1) Epibulbar dermoids and/ or lipodermoids
2) Auricular appendices and pretragal blind-ended-fistulas
3) Vertebral anomalies.
The facial anomalies in the Goldenhar syndrome represent defects in the embryonic first and second brachial arches,the first pharyngeal pouch and brachial cleft, and the primordia of the temporal bone.
There is no hereditary patterns, sex, or racial predilection.
Most cases are reported as unilateral, the right side most commonly involved.
When the condition is bilateral, one side is more severely affected than the other.
Patient of normal intelligence or mildly retarded.
Pathogenesis
Numerous hypotheses have been invoked explain the pathogenesis of this syndrome.
Stark and Saunders have invoked a theory of mesodermal deficiency. In which, there was insufficient mesodermal penetration of the first and second brachial arches.
Mckenzie has noted the possibility of an anomalous Stapedial artery as a cause of the embryonic failure.
Braithwaite and Watson attributed the facial anomalies to the aplasia or hypoplasia of the embryonic Stapedial artery.
The most attractive hypothesis has been proposed by Poswillo, whereby hemorrhage in the area of first and second arch may cause defects in the developing embryo.
An intrauterine hemorrhage of the stapedial artery, with hematoma formation may interfere with normal epithelial-mesenchymal tissue interactions and contribute to tissue necrosis.
The hemorrhage is believed to occur at approximately 6 weeks when the external carotid artery replaces the stapedial artery as the principal vascular supplier of the head and anterior neck regions.
Poswillo was able to reproduce hemifacial-like defects in monkeys with thalidomide and similar problems in mice with triazine.
Studies in both species demonstrated embryonic hematoma and destruction of differentiating mesenchyme.
In triazine- treated animals additional defects were noted in the vertebrae and ribs.
Clinical Features
The most comprehensive review of the clinical manifestations of the Goldenhar syndrome was presented by Gorlin and associates in 1963.
The principal facial deformity of the syndrome is focused on ototempromandibular region and from there radiates circumferentially to involve the middle and lower two thirds of the facial skeleton and the overlying soft tissue.
