OPTOMETRY. Short- and long-term vertical diplopia secondary to blunt trauma

Transcription

1 C L I N I C A L A N D E X P E R I M E N T A L OPTOMETRY Short- and long-term vertical diplopia secondary to blunt trauma Clin Exp Optom 2007; 90: 6: Philip RK Turnbull* Algis J Vingrys PhD Michael Kalloniatis* PhD * Department of Optometry and Vision Science, University of Auckland, New Zealand Department of Optometry and Vision Sciences, The University of Melbourne, Parkville, Australia m.kalloniatis@auckland.ac.nz DOI: /j x This report describes the short- and long-term ocular signs and symptoms of a patient with an orbital blow-out fracture and discusses the differential diagnosis of vertical diplopia. A blow-out fracture occurs when blunt trauma is applied either directly to the eyeball itself or the orbital rim and usually results in a fracture of the orbital floor with consequential excavation and entrapment of orbital contents in the fracture. Vertical diplopia is a common presenting symptom for a blow-out fracture of the orbit but careful considerations should be given to other potential conditions leading to such diplopia. A patient is presented who suffered a blow-out fracture almost a decade earlier, secondary to blunt trauma to the globe. The clinical findings are provided immediately after the trauma, post-surgery and during a recent ocular examination. Submitted: 11 December 2006 Revised: 20 March 2007 Accepted for publication: 22 March 2007 Key words: cranial nerve injuries, diplopia, eye injuries, orbital fracture A blow-out fracture of the orbit refers to conditions in which one or more of the bones that comprise the ocular orbit give way due to raised intraorbital pressure, usually due to blunt trauma. This case documents the short- and long-term follow-up of a blow-out fracture obtained during sport. While initial surgical intervention provided evanescent relief of diplopia, there was a progressive loss of the range of superior binocular single vision. This paper also reviews the aetiology and differential diagnoses of a blow-out fracture. CASE REPORT A 39-year-old male presented in December 1996, with a history of blunt trauma to his left eye and orbit caused by a punch, incurred during the State karate finals on the previous day. A laceration on the upper brow was surgically stitched a few hours after the injury. At presentation, he had swelling of the nose and periorbital ecchymosis extending inferiorly to the lip and gum on the left hand side. Vertical diplopia was reported in primary gaze immediately after eye opening following the blunt trauma. A bout of intense nose bleeding occurred approximately one hour after the injury and attempts to clear his nasal passages during the bleeding resulted in intense pain, to the point that the subject stopped blowing his nose. The subject monitored the vertical diplopia and had noticed that the degree of diplopia increased the further he looked in up-gaze but overall, the range of eye movements that resulted in diplopia had slightly decreased in the initial 24 hours. He had self-medicated with oral non-steroidal anti-inflammatory drugs (Celecoxib, 200 mg daily), immediately after the injury. He presented with an elevated chin, to sustain single vision and reported hypaesthesia on the upper left lip, left tip of the nose and upper frontal teeth consistent with involvement of the infra-orbital nerve. Vision was reported to be normal apart from the diplopia. Visual acuities were 6/4.8 right eye and 6/6 left eye with Van Herrick angle estimates of greater than 1.0 bilaterally. Intraocular pressure (IOP) was 14 mmhg in 457

2 Figure 1. Eye position in different gazes one day post-trauma. The left eye is depressed in primary gaze and the haematoma and smaller interpalpebral aperture are also evident. The marked restriction in the motility of the left eye is evident in up-gaze whereas eye positions are congruous in the three lower gazes. the right eye in all positions of gaze, whereas the left eye gave 20 mmhg in primary gaze, 27 mmhg in elevation and 18 mmhg in depression. The increase in IOP in up-gaze suggested a restrictive cause for the diplopia. Pupil reactions, extensive posterior pole evaluation and gonioscopy were all normal. Slitlamp examination was normal, in particular, there was no hyphaema Figure 1 shows eye position in nine gazes on the day after the trauma. In primary gaze, there is a clear depression of the left eye and a haematoma about the eye. The interpalpebral aperture is smaller on the left, partly due to chemosis of the surrounding tissues and to the enophthalmos (see measurements below). The restriction of the left eye is particularly evident in primary-, left- and up-gaze positions. Eye movements are full and normal in down-gaze. The region of visual space where diplopia existed was quantified using the Medmont perimeter and the Zone of Single Binocular Vision (BSV) test. This test presents points of light throughout the visual field and the patient is requested to look directly at them and determine whether they appear single or doubled. The patient responds to their percept with one or two button presses. The results show the region of diplopia and score the loss of single vision by weighting the inferior field more, given its importance for near. The Medmont BSV showed a reduction of 47 per cent of zone of single vision in superior left-gaze, which crossed the horizontal midline (Figure 2). Hess Screen testing confirmed the left hypo-deviation, which crossed over during depression. The following day, the patient returned for a review (three days post-trauma). Left eye acuity had recovered to right eye levels (6/4.8) and diplopia was subjectively reported to have improved. Pre-injury acuities in both eyes were equal at 6/4.8. Left eye intra-ocular pressures were 18 mmhg in elevation and 15 mmhg in primary gaze and depression. Right eye intraocular pressures were 15 mmhg in elevation and 13 mmhg in primary gaze and depression. The Medmont plot revealed a 31 per cent loss of BSV and showed no diplopia in primary gaze (Figure 2). The subject no longer adopted an elevated chin position. The enophthalmos was measured using a Luedde exophthalmometer and was found to be 17.5 mm right eye and 12 mm left eye. The subject was continuing to self-medicate with oral nonsteroidal anti-inflammatory drugs and was referred to an oculoplastic surgeon to investigate the possibility of a blow-out fracture of the orbit, likely to be involving the orbital floor. Management Although diplopia had improved, the fact that it had persisted required the patient to consult an oculoplastic surgeon for radiological assessment and management. Figure 3 shows four CT scan sections, indicating fracture of the floor of the orbit (maxillary bone) and ethmoid bone. The break in the floor of the orbit was extensive and located posteriorly: likely haemorrhaging is evident in the CT scan, showing a substance filling the ethmoid cavity (Figure 3B). Most surgeons agree that large fractures, enophthalmos and signs of entrapment are indications for surgery. In a survey among Australian and New 458

3 Zealand oral and maxillofacial surgeons (n = 113), most respondents stated that the proportion of fractures requiring exploration ranged from 50 to more than Post trauma 1 day 3 days Post surgery 5 days 11 days 3 months 90 months 90 months w/head tilt Figure 2. Medmont field of binocular single vision plots at different times after trauma and surgery. In primary gaze, diplopia extended below the horizontal plane but a dramatic improvement is seen within three days post-surgery. The minimal diplopia was experienced weeks after the surgery (for example, diplopia is experienced in only a few locations superiorly 11 days after surgery) but an increase was evident by three months. In primary gaze at 90 months post-surgery, diplopia has persisted in upper left gaze. The subject was asked to modify the chin position (down and to the right) to reveal the inferior locations where diplopia was also evident. In primary gaze, the nose prevented binocular vision and hence hid the diplopia present in inferior and to the right. 75 per cent. 1 Most (51 per cent) prefer to wait five to 10 days after the trauma before surgical intervention. Because of the impending surgery, the subject was instructed to terminate the non-steroidal anti-inflammatory medication because of the risk of haemorrhaging during and immediately after surgery. In this case, the floor of the orbit was repaired five days after the trauma, entering the orbit through an incision inferior to the globe. The patient was discharged after an overnight stay in hospital. A one-week course of oral antibiotics and topical chloramphenical were provided on hospital discharge. A mild conjunctivitis cleared within three to four days post-surgery. The patient resumed karate training within eight weeks of the surgery but wore protective goggles during sparing sessions. Only a minor degree of diplopia in elevation was evident five days post-surgery (11 per cent loss of BSV). This almost completely cleared 11 days post-surgery (Figure 2). The hypaesthesia involving the infraorbital nerve had worsened after the surgery, which is common due to the added surgically-induced trauma. The hypaesthesia slowly resolved over the next three months. A slight increase of diplopia was noticed on elevation and left-gaze over this same period (Figure 2). Apart from the occasional nose bleed (occurring at various times within the first three months post-surgery) and adjustment to the diplopia when the subject looked up and to the left, no other residual visual signs or symptoms remained. There is continued somatosensory hypersensitivity around the lateral canthus in the region surrounding the area where the surgical incision was made. The patient presented again at 90 months post-surgery because of persistent diplopia in up-gaze, occasional diplopia in primary gaze (particularly when there is reduced concentration) and presbyopic symptoms. Diplopia at 90 months was comparable to that at three months postsurgery (Figure 2). Stereopsis was measured at this time using a TNO stereogram at various angles of elevation relative to primary gaze. This showed a minimum angle of resolution of 15 in primary gaze, on depression (15, 30 ) and on 15 elevation. Stereopsis decreased to 60 of arc at 30 elevation. Of interest were vertical 459

4 Figure 3. CAT scans of the orbit beginning most posteriorly (A) and progressing forward in panel (D). The floor of the orbit is compromised in the most posterior aspects (panels A, B and C). A break in the lateral wall of the orbit (ethmoid bone) is particularly evident in panels B and C. The arrowheads in the different panels identify the breaks in the orbital bones. fusional reserves measured for the first time. The patient has no horizontal phorias at distance or near but displayed a very small (approximately 0.5 prism dioptres) right hyperphoria at distance and near (distance: von Graefe, near: Maddox wing). Vertical fusional reserves were asymmetric: 0.5 to 1 prism dioptres left hypo or right hyper and three to four prism dioptres left hyper or right hypo. The overall range is around five prism dioptres but the location of the ranges are markedly asymmetric. A presbyopic correction was prescribed. DISCUSSION The complaint of vertical diplopia has a well-established list of differential diagnoses including decompensated phoria, Myasthenia gravis, thyroid orbital diseases, mechanical interference of the globe or associated muscles, Brown s syndrome, skew deviation or paralysis of the third or fourth cranial nerves. 2 The cause for the initial presentation was obviously related to the trauma. It appeared to arise from a restrictive component prior to surgery. At 90 months post-surgery, the subject reported that diplopia was evident when looking up and to the left at all times but could be present in the primary position when tired or bored when listening to lecture presentations. Studies have shown that patients with long-standing vertical phorias tend to compensate for them and as a result have larger vertical fusional reserves 3,4 and may develop head tilts and better fusion vergences. Of note is Ansons and Davies s report 5 that many cases of orbital floor blow-out fracture have a temporary improvement with recurrence of the original restriction. Such recurrence appears likely in our case with a development of asymmetric vertical fusional reserves. Although this presentation arose from an obvious blow-out fracture of the orbit, more subtle trauma such as a bout of sneezing has been reported to also cause orbital floor damage. 6 A blow-out fracture of the left orbit would produce the left hypotropia with inability to elevate the left eye (Figure 1). A search for more subtle causes is needed to exclude cranial nerve involvement. Any palsy producing a vertical component should be assessed using the three-step test. A sixth nerve palsy does not produce vertical diplopia and will not be considered further. Cranial nerve palsies A palsy of the nerves innervating any of the four vertically acting muscles (the inferior and superior obliques and recti) could result in a vertical imbalance between the eyes and cause vertical diplopia. Innervating the superior oblique is the trochlear (CNIV) nerve, with the oculomotor nerve (CNIII) innervating the other vertical muscles, namely, the superior rectus, the inferior rectus and inferior oblique. CNIII also has branches to the medial rectus, levator palpebrae superioris, sphincter pupillae and the ciliary muscle. Therefore, a complete CNIII palsy results in the eye position becoming down and out, with accommodative paralysis, ptosis and a mydriatic pupil. 7 Rarely, the inferior division of CNIII (supplies the inferior oblique) can become entrapped in an orbital floor fracture

5 Third cranial nerve palsies are commonly caused by mass occupying lesions within the cranium, which compress the nerve at the level of the cavenous sinus. Ischaemic events along the nerve are another common cause of CNIII palsy. Traumainduced isolated CNIII palsies are rare due to its relative size compared to the other ocular nerves. Orbital closed-head injury may cause a partial CNIII palsy of one of the branches of the nerve, so full oculomotor function should be assessed with motility, lid, accommodation and pupil function. Considering these factors, a CNIII palsy is unlikely to be the problem in our case. CNIV is the only nerve to exit dorsally from the midbrain, which it does at the level of the inferior colliculi. It decussates completely at the posterior of the midbrain and has the longest unprotected path of the cranial nerves, which makes it particularly susceptible to closed-head trauma, 9 which is second only to idiopathic causes of palsies. 10 The nerve passes between the superior cerebella and posterior cerebral arteries, laterally to CNIII. Lesions can occur anywhere along the nerve from the midbrain to the orbit and cause contralateral superior oblique palsies. This results in vertical and torsional diplopia and horizontal diplopia when trying to converge and depress the eye, such as when reading. The gold standard clinical test for confirming a superior oblique palsy is the Park s Three Step test, in which each step reduces by two the number of potential muscles causing the vertical diplopia. 11 The first step asks Which eye has the hyper deviation in primary gaze?, which limits the affected muscles to the depressors of the hyper eye, or the elevators of the hypo eye. The second step is Does the vertical deviation increase with left or right gaze? As the deviation should increase when the eyes are turned in the field of the affected muscle, this reduces the possible muscles to an oblique muscle in one eye and the corresponding (inferior/superior) rectus muscle in the other eye. The third step takes into account the torsional ability of the oblique muscles or the unbalanced torsion in the case of an oblique palsy. For example, tilting the head to the left with a left fourth nerve palsy increases the vertical diplopia due to the unbalanced action of the inferior rectus extorsion, indicating a nonfunctioning superior oblique. Additional confirmation of a cyclotropia can be performed with a dual Maddox Rod test, offsetting the axes, by asking the patient to align the two lines. A result of greater than 10 degrees separation between the eyes indicates an abnormal result. If a bilateral CNIV palsy is suspected, the patient will show a very large V eso pattern, due to the limited ability of the eyes to abduct during depression. The patient may also report that the vertical diplopia is worse during near reading activities and that the torsional diplopia is greater when abducting. The Park s Three Step test would also show conflicting results the hypertropia manifests on the ipsilateral eye on both head tilt directions. In more subtle conditions where a blow-out fracture of the orbit may not be an obvious diagnosis (for example, sneezing causing a blow-out fracture), a Park Three Step test would be a useful adjunct to the examination. Additionally, direct trauma to the superior oblique muscle or trochlea could give the appearance of a fourth cranial nerve palsy. Blow-out fracture The orbit comprises seven bones: the maxilla, ethmoid, zygoma, lacrimal, palatine, sphenoid and frontal. The walls blow out either with direct force being applied to the front of the eye, such as being hit with a squash ball (hydraulic theory), or by larger objects hitting the strong orbital rim and deflecting the force backwards to the thinner orbital walls (buckling theory). The vast majority of blow-out fractures are of the orbital floor involving the superior portion of the maxillary bone. This comprises the floor of the orbit and is considered the weakest orbital bone due to its location overlying the maxillary sinus, thin wall and slightly angled (30 degree) inclination. 12 Less commonly affected is the ethmoid bone, which is also comparatively thin, or, rarely, the orbital roof. A blow-out fracture typically presents with periorbital ecchymosis from the traumatic event, vertical diplopia due to muscle or orbital tissue entrapment and eyelid swelling or pain after nose blowing due to communication between the maxillary sinus and orbit. The eye may be enophthalmic due to the collapse of the floor, though it may initially be proptotic due to intraorbital oedema. 13 Rarely, the medial rectus can entrap in the collapsed medial wall, causing horizontal diplopia and divergence problems. There may also be infraorbital hypaesthesia due to entrapment of the V2 branch of the trigeminal nerve. 12 This nerve traverses the floor of the orbit in the infraorbital groove so it is susceptible to damage in the event of an orbital blow-out fracture. It supplies the sensory innervation to the ipsilateral upper teeth, gums and lip, the cheek, lower eyelid and the side of the nose. As noted previously, many cases of orbital floor blow-out fracture may have a temporary improvement with recurrence of the original restriction. CONCLUSION The patient presented here is a classic case of blow-out fracture. The CT scan confirmed this diagnosis and gave the extent of the fracture. The marked elevation of intra-ocular pressure in the left eye on up-gaze one day post-trauma indicated restriction of the globe on attempted up-gaze consistent with inferior rectus entrapment. Day three post-trauma, the intra-ocular pressures were similar between the two eyes, indicating that the entrapment had subsided, although substantial eye movement limitation still existed. At this time, clear enophthalmos was evident as the swelling receded and the orbital contents began to settle into the fracture. One interesting aspect of this case was the remarkable improvement in binocular vision following surgery that lasted for about three months with subsequent recurrence of some restriction and diplopia in up and to the left gaze. Such recurrence is more likely in cases that sustain substantial damage to their orbits, as in this report, where both 461

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