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Blunt trauma & blow out fracture


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blunt ocular trauma and blow out fracture

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Blunt trauma & blow out fracture

  2. 2. Blunt Trauma Most common cause of blunt trauma are injuries from ball Anteroposterior compression with expansion in equatorial plane Transient increase in IOP Ocular damage can be in anterior or posterior segment
  3. 3. Cornea Corneal abrasion - Breach of the epithelium - Stains with fluorescein - Topical antibiotics and lubricants eye drops
  4. 4. Cornea Acute corneal oedema - Secondary to endothelium dysfunction - Descemet membrane folds resolve spontaneously - Descemet tears ( usually vertical )
  5. 5. Hyphaema Hemorrhage into the AC Source of bleeding is iris or ciliary body Red blood cells sediment inferiorly ( except in total hyphaema )
  6. 6. Hyphaema Total hyphaema Corneal Blood staining
  7. 7. Hyphaema May be associated with raised IOP (trabecular blockage by RBC ) Secondary hemorrhage ( more severe than primary bleed ) develop within 3-5 days of injury Sickle cell patients at increased risk
  8. 8. Hyphaema Risk of Glaucoma Prolonged elevation of IOP – - ON damage - Corneal blood staining Size of hyphaema ( indicator of prognosis ) 1. Less than half AC – - 4% incidence of raised IOP - 22% incidence of complications - Final VA of more than 6/18 in 78% eyes
  9. 9. Hyphaema 2. More than half AC – - 85% incidence of raised IOP - 78% incidence of complications - Final VA of more than 6/18 in 28% eyes MANAGEMENT – Coagulation profile – BT, CT, Early and late Sickling Stop any anticoagulant medication after physician opinion Limited activity and semi-upright position
  10. 10. Hyphaema MEDICAL Treatment – - Anti-Glaucoma drugs - Beta-blocker or Carbonic anhydrase inhibitor ( topical or systemic ) depending on IOP - Prevent CAI in sickle cell - Avoid :- 1. Miotics – may increase pupillary block 2. Prostaglandins- promote inflammation 3. Alpha agonist – small children and sickling Hyperosmotic agents may be needed
  11. 11. Hyphaema Topical steroids – reduce inflammation Mydriatics ( controversial ) - Atropine recommended - Constant mydriasis ( rather than a mobile pupil ) - Minimize chances of secondary haemorrhage Systemic antifibrinolytics ( aminocaproic acid or tranexamic acid ) – rarely given
  12. 12. Hyphaema SURGICAL :- Indication – IOP of 25mmHg or more for 5 days with total hyphaema IOP of 60mmHg or more for 2 days - Surgical evacuation of blood - Prevent Optic atrophy - Risk of permanent corneal staining - Development of PAS - Hemoglobinopathy - Children with risk of amblyopia
  13. 13. Anterior Uvea PUPIL :- - Compression of iris against anterior surface of lens - VOSSIUS RING - Imprinting of pigments from pupillary margin - Transient miosis occurs due to compression - Pigment pattern corresponds to miosed pupil
  14. 14. Pupil Damage to iris sphincter – Traumatic mydriasis - Pupil reacts sluggishly or not at all Radial tears are also common in pupillary margin
  15. 15. Iridodialysis Dehiscence of iris from the ciliary body at its root D-shaped pupil Symptoms- Uniocular diplopia, glare May be asymptomatic is covered by Upper lid
  16. 16. Iridodialysis  A cataract surgery–type incision is made at the site of iridodialysis or iris disinsertion A double-armed, 10-0 polypropylene suture is passed through the iris root, out through the angle, and tied on the surface of the globe under a partial-thickness scleral flap. The corneoscleral wound is then closed with 10-0 nylon sutures
  17. 17. Iridodialysis Alternative technique Multiple 10-0 Prolene sutures on double-armed Drews needles are passed through a paracentesis opposite the site of iris disinsertion to avoid the need to create a large corneoscleral entry wound
  18. 18. Iridodialysis Traumatic aniridia can also occur ( 360* Iridodialysis ) Special scleral fixating IRIS LENS can be used
  19. 19. Aniridia
  20. 20. Ciliary Body and IOP IOP should be monitored carefully Elevation can occur – hyphaema or inflammation Hypotony –Temporary cessation of aqueous secretion ( Ciliary shock ) Exclude open globe injury Angle recession – Tears extending into face of ciliary body ( risk of glaucoma )
  21. 21. Angle recession Rupture of face of the ciliary body Rise in IOP secondary to associated trabecular damage Risk of glaucoma depend on extent of recession Glaucoma may not develop until months to years after injury Gonioscopy – Irregular widening of ciliary body Absent or torn iris processes White glistening scleral spur Depression in the overlying TM Localized PAS at the border ofthe recession Long standing cases , fibrosis and hyperpigmentation
  22. 22. Gonioscopy
  23. 23. Angle Recession Medical Treatment Secondary open angle glaucoma Unsatisfactory Laser trabeculoplasty is ineffective Trabeculectomy – with antimetabolite, effective Artificial filtering shunt – if trabeculectomy fails
  24. 24. Lens CATARACT-  common Mechanisms:- - Damage to lens fibres - Rupture of anterior capsule – influx of aqueous – hydration of lens fibres- opacification Ring shaped anterior capsular opacity Posterior subcapsular cortex ( flower shaped ‘ Rosette’ opacity ) is common
  25. 25. Rossete shaped Cataract
  26. 26. Subluxation Tearing of suspensory ligaments Deviate towards intact zonules AC may deepen over the area of dehiscence Phakodonesis may be seen on ocular movement Symptoms- uniocular diplopia lenticular astigmatism ( tilting )
  27. 27. DISLOCATION:- 360* zonular rupture Into vitreous or AC ( rare )
  28. 28. GLOBE RUPTURE Commonly anterior In vicinity of Schlemm canal Prolapse of -Lens -Iris -Ciliary body -Vitreous May be masked by extensive SCH
  29. 29. GLOBE RUPTURE Posterior rupture - May be little damage to AS - Asymmetry of AC depth - Hypotony - If enucleation is not performed, eventual shrinkage of the globe will occur resulting in phthisis bulbi.
  30. 30. Vitreous Hemorrhage and PVD Often associated with Posterior vitreous detachment TOBACCO DUST – pigment cells seen floating in anterior vitreous
  31. 31. Commotio Retinae/Berlin oedema Concussion of sensory retina, cloudy swelling Common in temporal fundus If macula involved- ‘Cherry-Red spot’ Sequelae to more severe form- macular hole
  32. 32. Chorioretinitis Sclopetaria Simultaneous break in the retina and choroid High velocity object Reveals bare sclera Often surrounding commotio retina present Surrounding area develop scar formation with time May progress to VH or retinal detachment ( require vitrectomy and/or scleral buckling )
  33. 33. Choroidal Rupture Involves choroid, Bruch membrane, RPE Types - Direct or Indirect Direct rupture- located anteriorly - parallel with ora serrata Indirect rupture- opposite site of impact Fresh rupture obscured by subretinal hemmorhage
  34. 34. Choroidal Rupture On absorption of blood ( weeks to months ) White crescentic vertical streak of exposed sclera seen Late complication- choroidal neovascularisation
  35. 35. Traumatic Choroidopathy RPE contusion results in RPE damage and leakage Leakage can result in serous RD ( resolve within three weeks ) VA is often normal if foveal area is spared FFA- multifocal areas of leakage at level of RPE No treatment
  36. 36. Retinal breaks and detachments 10% retinal detachments are due to trauma Most common cause in children RETINAL DIALYSIS :- Most common in superonasal and inferotemporal quad Break occuring at ora serrata Traction of inelastic vitreous gel along posterior aspect of vitreous base BUCKET HANDLE appearance- strip of ciliary epithelium, ora serrata and immediate post oral retina
  37. 37. Dialysis
  38. 38. Retinal Breaks and Detachments Equatorial breaks:- - Less common - Direct retinal disruption ( point of scleral impact ) - Treatment is by laser therapy to prevent RD Macular hole:- - At time of injury - Following resolution of commotio retinae
  39. 39. Optic Nerve Traumatic optic neuropathy ( TON ) - Present as sudden visual loss Types – 1. Direct – blunt or sharp injury 2. Indirect – secondary to impacts - Eye, orbit, cranial structures
  40. 40. TON Mechanisms:- - Contusion - Deformation - Compression or transection of nerve - Intraneural hemorrhage - Shearing force - Secondary vasospasm - Oedema
  41. 41. TON Presentation :- VA usually poor PL in 50% cases Optic nerve and fundus appears normal initially Only finding is afferent pupillary defect
  42. 42. TON MANAGEMENT :- Megadose corticosteroids Administer within 8hrs after injury Antioxidant, membrane stabilizing Increased microcirculation Methylprednisolone 30mg/kg iv over 30 mins followed by 15mg/kg 2 hours later Continue with 15mg/kg every 6 hours for 24-48 hours If visual function improves,taper If no improvement , optic canal decompression
  43. 43. TON CRASH Trial Corticosteroid Rnadomization After Significant Head Injury Showed increased mortality among patients with acute head trauma who were treated with high-dose corticosteroid
  44. 44. Optic Nerve Avulsion Rare Sudden extreme rotation or anterior displacement of globe Fundus – shows cavity where ONH has retracted from dural sheath
  45. 45. Blow-out fractures ORBITAL FLOOR:- - Sudden increase in orbital pressure - Impacting object with diameter greater than orbital aperture ( Fist , tennis ball etc ) - Eye ball gets displaced and transmits the impact fracturing the thinnest Orbital Floor - Occasionally also the medial wall - Pure Blowout fracture – orbital rim not involved - Impure Blowout fracture – involve rim and/or adjacent facial bones
  46. 46. Signs and Symptoms Periocular signs – - Ecchymosis - Oedema - Subcutaneous emphysema
  47. 47. Signs and Symptoms Infraorbital Nerve anaesthesia – Due to involvement of infraorbital canal - Lower lid - Cheek - Side of nose - Upper lip - Upper teeth - Gums
  48. 48. Signs and Symptoms Diplopia :- Mechanisms- 1. Haemorrhage and oedema - Restrict movements of IR and IO - Motility improves with time
  49. 49. Signs and Symptoms Diplopia:- 2. Direct injury to muscle Negative FDT Muscle fibres regenerate ( 2 months ) 3. Mechanical entrapment- - Within the fracture ( IR, IO, Connective tissue, fat ) - Double diplopia ( up and down gaze ) - FDT positive - Improves if connective tissue and fat is entraped
  50. 50. Signs and Symptoms Enophthalmos :- - Mostly with severe fracture - Manifest after edema subsides - May progress for 6 months due to degeneration and fibrosis ( if no surgical intervention )
  51. 51. Signs and Symptoms Ocular Damage - Should be excluded by SLE and Fundus Radiological Findings :- - Coronal section - Maxillary antral soft tissues - Prolapsed orbital fat ( Tear drop sign ) - EOM - Haematoma
  52. 52. Tear Drop Sign
  53. 53. Treatment Initial Treatment :- - Antibiotics - Ice packs - Nasal decongestants - Systemic steroids ( severe oedema compromising ON ) - Not to blow nose
  54. 54. Treatment Further management aimed at prevention of – - Permanent vertical diplopia - Cosmetically unacceptable enophthalmos - Factors determining risk of above complication:- 1. Fracture size 2. Herniation into maxillary sinus 3. Muscle entrapment
  55. 55. Treatment No Treatment required - 1.Small cracks without herniation 2.Fracture involving upto 1/3rd of floor + little or no herniation + no enophthalmos + improving diplopia Treatment required – - More than 1/3rd of floor ( develop significant enophthalmos if untreated )
  56. 56. Treatment Treatment within 2 weeks- - Entrapment of orbital contents + enophthalmos greater than 2mm + significant diplopia in primary gaze - If surgery delayed – result less satisfactory because of fibrotic changes
  57. 57. Trap Door effect Aka white-eyed fracture In patients less than 18 years of age Little visible external soft tissue injury Greater elasticity of bone Acute incarceration of herniated tissue Symptoms :- - Acute nausea - Vomiting - Headache - Oculo-cardiac reflex
  58. 58. Trap-door effect CT – shows intact floor Urgent treatment required – - Prevent permanent neuromuscular damage - Early marked enophthalmos
  59. 59. Surgery Transconjunctival or subciliary incision ( 3mm below lash margin ) Dissect orbicularis, avoid injury to infraorbital nerve Periosteum is elevated from floor and entraped content removed Defect in floor repaired by – - Supramid - Silicone - Teflon No implant – if fracture is linear, small, trap door Periosteum sutured
  60. 60. Blow-out medial wall fracture Fracture of medial wall with intact orbital rim Rarely isolated Usually associated with floor fracture Signs/Symptoms :- - Periorbital ecchymosis - Subcutaneous emphysema ( blowing nose ) - Defective abduction Plain Radiograph – Water’s and Caldwell view – show clouding of ethmoidal air sinus
  61. 61. Surgery Two approaches- 1.Lynch incision- over superomedial orbital rim - excellent exposure - lacrimal sac separated from fossa - Ethmoidal vessels coagulated Disadvanatge - severe scarring 2.Transcaruncular approach- avoids a visible scar
  62. 62. THANK YOU