Orbital complications of ZMC fracture

1. ORBITAL COMPLICATIONS IN
ZYGOMATIC FRACTURES
Presented By:
Dr. Mrinalini Mathur
Moderated By:
Dr. Parul Tandon(Reader)

2. DIPLOPIA

3. Diplopia
Our two eyes work mutually; the images
that hit the fovea are processed by the
brain. Thus the term Binocular single
vision is used. In the absence of
simultaneous perception of light from the
same object, the binocular single image is
not formed. It is the result of impaired
function of Extraocular Muscles. Problem
with the extraocular muscle could be
Mechanical(Trauma & Injury), Disorder of
Motor neuron- Muscle
junction(myoneural junction), Disorders
of trochlear, Abducens, & Oculomotor
cranial Nerve.

4. Classification
-Binocular Diplopia
-Monocular diplopia
-Temporary Diplopia
-Voluntary Diplopia
Causes
-Corneal irregularities
-Sjogren's syndrome(Severe Dry Eye)
-Muscle entrapment
-Nerve palsy
-Refractive surgery

5. Check For Diplopia

7. Determine The Cause

8. Diplopia Charting
Diplopia chart is the record of subjective separation of double images in the
nine positions of gaze.
Two methods
1. Simple method
2. Electronic devices(Hess n Lees screens )

9. Simple Method
-Patient comfortable with his head erect and should preferably be still throughout
the examination.
-Carried out in a dark room.
-A red glass is put in front of one of the eyes (red in front of right, R for R, is a
convention). It is desirable to use Armstrong goggles since these are shaped to fit
the orbital margin.
-Examiner holds the torch at around ½ m or 1 m (It is important to mention the
distance on the chart).The light is held directly in front of the patient at first. If the
patient notes a double image, the relative position of these images is noted.

10. -The light is then carried to the other 8 positions of gaze.
-If there is no double vision in primary position, the position in which double
vision appears and is maximal is to be noted.
-In each gaze position the patient must be asked whether the images are,
parallel , distance between two images & tilt if present.
-Colored pencils can be given to patient to show the separation.

12. Analysis of diplopia
Rules governing the relationship of two images
RULE 1.Displacement of the false image may be horizontal or vertical or both.
RULE 2 : Separation of the 2 images is greatest in the direction in which the weak
muscle has its purest action.
RULE 3: False image is displaced furthest in the direction in which the weak muscle
should move the eye.
RULE 4: The distal image ( image that is farthest away ) belongs to the paretic eye
RULE 5: If the images are exactly side by side it will be only the lateral or medial recti
that are involved.
RULE 6: If they are one above the other, either of the obliques, or the superior and
inferior recti, may be defective.

13. Hess Screen
-Walter Hess,1908.
-Principle is haploscopic – based on Burian principle – that in presence of normal
retinal correspondence, the two test objects presented to the two eyes will be
superimposed if they stimulate foveae of the two eyes, irrespective of the position
of the two eyes.
-Chart is plotted based on the Hering’s and Sherrington’s law of innervation.
-Dissociation of two eyes is by the means of colors.
-Haploscopic principle: two targets, one target pointed and patient has to
superimpose it with other target.

14. -Herings law of equal innervation: an equal and simultaneous innervation flows from
the brain to pair of muscles of both eyes (yoke muscle) which contract simultaneously
in different binocular movements.
-Sherrington's law of reciprocal innervation states that: When a muscle contracts, its
direct antagonist relaxes to an equal extent allowing smooth movement.
-Original Hess screen is a single tangent screen made up of a black cloth 3 feet height
and 3 feet long, marked by horizontal and vertical lines.
-Chart includes horizontal and vertical lines that subtend a visual angle of 5 degree.
-Fixation points are indicated at the centre of the screen and at the intersections of 15
deg and 30 deg lines by red dots. The screen is used to map/ chart the relative
positions of each eye in 9 gazes
Inner 15 degree field – 8 dots ( testing points )
Outer 30 degree field- 16 dots ( testing points )
After all the points are plotted – dots are joined by lines to identify inner and outer
field.

16. -Test is performed with each eye fixating in turn.
-It is done at 50cm.
-Patient wears red and green glasses
-Eye to be tested should have green glass in front of it.
-The chart has electronically operated board with small red lights. Patient is asked to
place green light in each of points on red light as illuminated.
-When red light controlled by the examiner
• Eye under RED goggle acts as the Fixing Eye
• Eye under GREEN goggle acts as the Indicator Eye

17. -The patient wears red-green goggles and is seated 50
cm from the screen, preferably with his or her head
fixed in a headrest.
-The patient now sees the red dots with one eye (fixing
eye) and the green cords with the other (charted eye).
-The patient is instructed to place the three green cords
over each of the red dots in screen.
-It is advisable to start from point A then go to above
point B then proceed clockwise from C to I.
-The points found by the patient are connected by
straight lines and permit the examiner to determine
which, if any, muscles react abnormally.
-To change fixation, the red green goggles are reversed
with the red filter now in front of the left eye.

18. Hess Chart(Position)
-The basic principle of Hess
chart is foveal projection
therefore the higher field
belongs to the higher eye.
-Position of the central dot
indicates whether the deviation
is in primary position or not.

19. Hess Chart(Size)
-The variation in the size of the Hess
chart of each eye is due to the
Hering’s law.
-Small field belongs to the eye with
primary limitation of movement.
-Underaction can be seen with the
inward movement of the dots and
therefore the whole curve.
-Overaction can be seen by noting
the outward displacement of the
dots.

20. Hess Chart(Shape)
-Each small square on the grid subtends
5 degree at the working distance of 50
cm. Therefore the amount of deviation
can be calculated.
-In primary position, the amount could
be calculated by fixing either eye by the
displacement of the pointer from the
centre dots.
-The amount of underaction and
overaction can be calculated in the
various positions and hence the amount
of excursions can also be calculated.

21. Causes of III, IV and VI nerve palsies
Site Common causes
Brain stem • Stroke Superior orbital fissure • Tumor
• Demyelination
Meningeal • Meningitis Orbit • Infection
• Raised ICT • Tumor
• Aneurysms • Trauma
• Cerebellopontine angle tumor
• Trauma
Cavernous sinus • Infection
• Thrombosis

22. 3rd nerve palsy
-Complete 3rd nerve lesion causes total paralysis
of the eye lid, so diplopia occurs only when the lid
is held up.
-When the lid is lifted the eye will be found
deviated outwards and downwards.
4th nerve palsy
-Principal action of the muscle is depress and
intort globe– palsy of it causes hypertropia
and excyclotorsion.
-Head Tilt test : Vertical diplopia is seen upon
reading or looking down– exacerbated by
tilting the head towards the side with muscle
palsy and alleviated by tilting away.
( Cardinal diagnostic feature)

23. 6th nerve palsy
-Abducens nuclear lesion produces a
complete lateral gaze palsy from
weakness of both ipsilateral lateral
rectus and contralateral medial rectus.
-UL/BL abducens palsy is a classic sign
of raised intracranial pressure.
-Diagnosis is confirmed by papilladema
(Fundus).

25. Management
Patching ( occlusive ) therapy
Identify and treat the underlying cause of the problem
Eye exercises
Wearing an eye patch on alternative eyes
Prism correction
Surgery
Botulinum toxin

26. ENOPHTHALMOS

27. Enophthalmos
Retro positioning of the globe in its three dimensional relationship in the orbit.
• Should always be assessed in relation to the contralateral eye
• It is an unsightly deformity which can be impossible to correct completely
• Regarded as the most common and serious sequalae of complex orbital
trauma.

28. Signs And Symptoms
• Sunken eye
• Narrowing of palpebral width with pseudo-ptosis of the upper lid
• Supra tarsal hollowing
• Hooding of the eye
• Decreased anterior projection of the globe
• Paresthesia of the infraorbital nerve

29. Categories
• No enophthalmos
• Mild enophthalmos <2mm
• Moderate enophthalmos 3-4mm
• Severe enophthalmos >4mm

30. Causes
• Increased orbital volume
• Herniation of orbital fat
• Orbital fat atrophy
• Loss of ligamentary support
• Trochlear dislocation
• Entrapment of tissues in blow outs pulls the whole system downwards and backwards
• Action of gravity on orbital contents in an enlarged cavity

31. Relationship With Orbital
Volume
• 1mm medial displacement of the medial wall results in a 0.4 ml increase in orbital
volume.
• 1mm inferior displacement of the floor results in a 0.8 ml increase in orbital volume.
• An increase in orbital volume of approximately 1.25 ml will result in 1mm enophthalmos.
• 10% (2.5ml) increase in volume would be expected to result in clinically significant
enophthalmos.
• This is roughly equivalent to 3mm inferior displacement of the orbital floor.

32. Clinical Examination
ASSESS
• Visual acuity
• Eyelids and periorbital regions
• Extra-ocular movements
• Pupillary light reactivity
• Globe projection
• Measure enophthalmos with Hertel’s or Naugle’s exophthalmometer
• Paraesthesia
• Canthal positions
• Eye and ZMC symmetry in all three planes

33. HERTEL EXOPHTHALMOMETER NAUGLE EXOPHTHALMOMETER
Among adults, the usual
distance from the lateral
orbital
rim to the corneal apex is
approximately 16-21mm.

34. Investigations
• OM 15° and 30°
• CT (axial/coronal) 3-5mm slices
• 3D CT

35. Surgical Approaches
• Subciliary / Subtarsal
• Transconjunctival with / without lateral canthotomy
• Infra orbital
• Lateral nasal approach for medial wall
• Coronal
• Endoscopic Intra sinus

36. Indications For Surgery
• Enophthalmos of 2mm or more present for 2 weeks
• Positive forced duction test (FDT)
• Volume expansion on CT scan
• Herniation of orbital contents in the maxillary antrum
• Combined medial and inferior wall fracture
• Isolated medial wall fracture with displacement >3- 5mm
• Isolated floor fracture with displacement > 3mm
Early intervention is always beneficial as late intervention gives poor results
because of extensive scarring and muscle shortening.

37. Aims Of Surgery
• Restore anatomy
• Restore orbital volume
• Preserve vision
• Improve eye movements
• Restore esthetics

38. Management
ENOPHTHALMOS WITH ISOLATED ORBITAL FRACTURES
• Expose the fracture site
• Free all the entrapped and herniated tissue
• Wide subperiosteal exposure
• Find a fixed base posterior to the globe
• Reconstruct the defect with graft or plate
• Graft or plate should fit passively and must be fixed to the base or rim with
plates/screws
• Graft must be placed behind the globe axis to push it forward
• Assess with FDT again before closure
• Close in layers

39. ASSOCIATED ZMC FRACTURES
• Expose the fracture sites
• Reduce the displaced ZMC and the fractured rims to their accurate anatomical
positions
• Rigidly fix ZMC (3 point fixation)
• Free any herniated tissue
• Graft/plate any defects
• Perform FDT before closure
• Close in layers

40. Complications
• Failure to correct properly in the initial setting thus requiring secondary repair
• Iatrogenic damage to the globe
• Optic nerve compression
• Graft resorption and recurrence of enophthalmos
• Infection/extrusion of the graft/plate
• Foreign body reaction
• Tissue sagging owing to inadequate closure
• Scarring, ectropion or scleral show

41. RETROBULBAR
HEMORRHAGE

42. Massive retrobulbar hemorrhage in the posterior region of the muscle cone, triggered
by vessel disruption, leads to progressive exophthalmos with concurrent pupil
dilatation, reduced vision and increased intraocular pressure. (Ord 1981; Ord and El
Altar 1982)
Retrobulbar hemorrhage may occur spontaneously or as a result of trauma, peribulbar
or retrobulbar injections, or surgery.
A Retrobulbar hemorrhage is a space-occupying lesion of the orbit leading to forward
displacement of these structures as intraorbital volume and pressure increases.
Neurological damage is caused by direct compression, by bony fragments or by an
indirect compression of the nerves caused by hemorrhage (Rowe and Williams 1985)

43. Etiology
Spontaneous : Orbital vascular abnormality Arteriovenous malformation
Uncontrolled hypertension Scuba diving, weightlifting, sneezing
Post Traumatic : Orbital Fractures
High Level Midfacial Fracture
Le Fort III Fracture
Post Anaesthesia : Retrobulbar injection
Peribulbar injection
Sub-Tenon’s injection(episcleral)
Post Operative : Facial /Orbital Fracture Repair
Endoscopic Sinus Surgery

45. Soft Tissue Considerations
The orbit is lined by periosteum that attaches firmly at the foramina, fissures, suture
lines and the posterior lacrimal crest. Between these firm attachments the
periosteum is loosely adherent, creating a potential space for accumulation of blood.
The characteristic CT appearance of an acute subperiosteal hematoma is a broad-
based extraconal mass that abuts the bony orbit and displaces orbital contents
centrally. Radiographically, the mass is high-density, sharply defined and
homogeneous.

46. All mechanisms relate to increased intraorbital pressure and volume leading to:
:Ischemic optic neuropathy from compression or stretching of the small nutrient vessels
:Direct compressive optic neuropathy
:Central retinal artery occlusion
:Retinal vascular ischemia

47. Signs And Symptoms
-Protrusion of the globe (up to 10 mm)
-Increased intra-ocular pressure more than 80 mmHg
-Ischemia of the optic disk and retina with clearly reduced vision
-Pain
-Reduced vision
-Diplopia

48. -MRI scans provide better visualization of the soft tissues of the orbit.
-CT scans are preferred because of their fast acquisition time and better visualization
of the bony anatomy.
Investigations

49. Treatment Options
-Once the diagnosis is made, therapy should begin immediately.
-Optic nerve damage was proportional to the duration of occlusion of Central Retinal
Artery.
-Treatment is aimed at lowering intraorbital or intraocular pressure and protecting the
optic nerve from damage.
-Rapid surgical intervention remains the mainstay of treatment.

50. Medical Treatment Options
Include
Oxygen therapy: May decrease the ischemic insult by dilating intraocular vessels.
Mannitol 20% IV: The hyperosmotic agent, rapid IV infusion of 1.5 - 2 g/kg over 30 min,
with the first 12.5 g over the first 3 min. Reduces intraocular pressure.
Acetazolamide: The carbonic anhydrase inhibitor. Given 500 mg IV. Lowers intraocular
pressure.
Steroids: Methylprednisolone, 100 mg, decrease inflammation and edema.
Topical β-blockers: Decrease intraocular pressure by lowering aqueous humor
secretion.

51. Surgical Treatment

52. -Relieve orbital compression primarily.
-Can often be achieved via a lateral canthotomy and inferior cantholysis.
-If further decompression is needed, a lateral anterior orbitotomy may be required to
break the fibrous septa of the orbital fat compartments.
-Pterional orbital decompression:A neurosurgical approach.
Removal of the bony lateral and superolateral orbital walls to maximally decompress the
orbit

53. Post-operative Care
-The patient must be closely followed with serial examinations:
Pupillary light reflexes
Visual acuity
Intraocular pressure
Fundoscopy
-The head of the bed may be elevated to decrease arterial pressure.
-The lateral canthotomy and cantholysis may be repaired days later to allow for
further drainage in the event of additional hemorrhage or it may be allowed to heal
spontaneously.

54. THANK YOU