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Ophthalmic Injuries
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Outward displacement of the orbital walls (blow-out fractures) can produce enophthalmos (a sunken eye). Alterations to bone position may in turn alter globe position by changing the manner of muscular insertion. Hypoglobus (inferior globe displacement) is the most common non-axial type of globe displacement and is associated with a fracture of the orbital floor. Subluxation of the entire globe into the maxillary sinus has been described in extreme orbital floor disruption.8
The nervous system
Published in Peter Kopelman, Dame Jane Dacre, Handbook of Clinical Skills, 2019
Peter Kopelman, Dame Jane Dacre
Horner’s syndrome This is due to paralysis of the cervical sympathetic chain. It consists of slight drooping of the eye (ptosis), pupillary constriction, absence of pupillary dilatation on shading the eye and absence of sweating on the corresponding half of the face and neck (Fig. 6.41). Enophthalmos (apparent indrawing of the eye) is often also present. The pupil of a completely blind eye is dilated and fails to react to light, but it constricts when light is shone into the opposite normal eye.
Orbital trauma
Published in John Dudley Langdon, Mohan Francis Patel, Robert Andrew Ord, Peter Brennan, Operative Oral and Maxillofacial Surgery, 2017
Although there are four walls at the orbital rim, further back in the orbit the medial wall and floor blend together; at this point, the orbit becomes a three-walled pyramidal structure. This blending of the medial and lateral wall forms an important postero-medial bulge which has also been coined the ‘key area’. This is an important area to replicate in orbital reconstruction to minimize post-operative enophthalmos. The anterior and posterior ethmoidal arteries pass through the medial wall and are important surgical landmarks. Passing through the floor is the inferior orbital fissure which contains no structure of surgical importance.
Multimodal Imaging of Parry Romberg Syndrome-associated Panuveitis: A Case Report and Review of Literature
Published in Ocular Immunology and Inflammation, 2021
Jialiang Duan, Minhao Li, Qiannan Chai, Nalei Zhou, Yuhua Hao
Parry-Romberg syndrome (PRS), also known as progressive hemifacial atrophy, is a rare disease characterized by unilateral facial atrophy with unknown etiology.1 Only a subset of patients develops secondary ophthalmologic symptoms; while these vary in manifestation, enophthalmos is reportedly the most common.1,2 Other ocular findings associated with PRS include exposure keratopathy, spontaneous scleral melting, hypotony, Coats’ disease, and retinitis pigmentosa.2–4 However, few reports have documented the comorbidity of PRS with intraocular inflammatory disease. We present a patient with PRS with panuveitis and retinal vasculitis, which was subsequently analyzed with multimodal imaging. In addition, we provide a literature review relevant to PRS associated with intraocular inflammation is presented.
Post-traumatic enophthalmos secondary to orbital fat atrophy: a volumetric analysis
Published in Orbit, 2020
Liza M. Cohen, Larissa A. Habib, Michael K. Yoon
Collective clinical experience has shown that for generally accepted indications for orbital fracture repair (early enophthalmos, “large” fractures, diplopia within 15 degrees of primary gaze), successful surgical outcomes are frequently achieved, restoring globe position and improving diplopia. However, in patients with late enophthalmos, the rate of success has been generally lower, prompting investigations into why.8 Orbital fat atrophy secondary to post-traumatic enophthalmos may occur via various mechanisms, though no conclusive cause is known. Ramieri et al., who found a non-significant decrease in fat volume in enophthalmic orbits, speculated that fat atrophy is likely compensated for by scar formation and is typical in cases with posterior orbital fractures.2 Additionally, in a review of CT imaging characteristics in patients with orbital fractures, Kim et al. found that soft tissue incarceration/injury was the only factor that increased the risk of developing late enophthalmos.9 Blunt trauma to the orbital fat, as occurs with orbital fracture, may induce fibrosis and atrophy. In addition, fat displacement, increase in total orbital volume, loss of ligamentous support, and fibrosis of soft tissues are other factors that have been speculated to play a role in post-traumatic enophthalmos.9,10 Further studies in this area are needed to fully elucidate the etiology of post-traumatic enophthalmos.
Management of pediatric orbital wall fractures
Published in Expert Review of Ophthalmology, 2019
The patient history and examination offer clues regarding the presence of an orbital fracture with or without incarceration of the orbital soft tissues. Periorbital ecchymosis, laceration, edema, and subconjunctival hemorrhage suggest an injury capable of producing a fracture. Palpation may reveal step-off of the orbital rim, crepitus, and hypoesthesia in the distribution of the infraorbital nerve (ipsilateral malar surface and upper lip). The patient may report malocclusion or trismus in the case of a more extensive fracture. Lateral canthal dystopia and flatness of the malar prominence is suggestive of a trimalar fracture. Exophthalmometry may reveal either proptosis from coexistent orbital edema and/or retrobulbar hemorrhage or enophthalmos due to increased orbital volume. Enophthalmos may be initially masked by orbital and periorbital edema. Eye movements may be reduced either from edema and hemorrhage or as a result of entrapped orbital tissues within the fracture. A limitation of upgaze, however, is suggestive of entrapment. The practitioner must remember that children may present with little or no signs or symptoms of entrapped or nonentrapped orbital fractures.