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Ocular trauma

This document provides an overview of ocular trauma and basic management principles. It begins with an introduction on the importance of the eyes and prevalence of ocular trauma. It then covers epidemiology, classifications using the BETTS system, evaluation of patients, investigations, general management principles, and management of specific injuries such as closed globe, open globe, lid injuries and subconjunctival hemorrhage. The document aims to outline the evaluation and basic management of common ocular trauma presentations.

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OCULAR TRAUMA AND BASIC MANAGEMENT PRINCIPLES By Dr. Amreen Deshmukh Under Guidance of Dr. K. G.Choudhary Sir
Outline  Introduction  Epidemiology  Classification  Evaluation  General principles  Management of individual conditions  Complications  Prevention  Conclusion
Introduction  It is said that “ Eyes are window to the soul and to the outer world.”  Ocular trauma is a major cause of preventable monocular blindness and visual impairment in the world, especially in the developing countries  Ocular trauma and resultant loss of vision leads to psychological, economical and professional crippling of the patient.
Epidemiology  Bimodal age distribution: children and young adults;>70 yrs of age  M/F: 3-5x  Lifetime prevalence 20%: 3x recurrence risk  workplace, sports, falls(elderly)  PUBLIC HEALTH ISSUE
 TheWHO Programme for the Prevention of Blindness, suggests that annually  55 million eye injuries restricting activities more than one day  750,000 cases will require hospitalization  200,000 open-globe injuries  approximately 1.6 million blind from injuries  2.3 million people with bilateral low vision  19 million with unilateral blindness or low vision.
Classification of Ocular Trauma  The Birmingham EyeTraumaTerminology System (BETTS) devised a classification for ocular trauma which is accepted worldwide.  It is unambiguous, consistent and simple.
Eye Injury ClosedGlobe Contusion Lamellar Laceration Open Globe Rupture Blunt trauma Laceration Penetrating Injury IOFB Perforating Injury BETTS Classification
Open Globe Injury Classification  Type 1. Rupture 2. Penetrating 3. Intraocular 4. Perforating 5. Mixed  Grade- visual acuity 1. ≥20/40 2. 20/50 to 20/100 3. 19/100 to 5/200 4. 4/200 to light perception 5. No light perception  Pupil  Positive-RAPD+ in affected eye  Negative-No RAPD in affected eye  Zone I. I- Isolated to cornea (Including the corneoscleral limbus II. II- Corneoscleral limbus to a point 5mm posterior into the sclera III. III- Posterior to anterior 5mm of sclera
Closed Globe Injury Classification  Type 1. Contusion 2. Lamellar laceration 3. Superficial foreign body 4. Mixed  Grade- visual acuity 6. ≥20/40 7. 20/50 to 20/100 8. 19/100 to 5/200 9. 4/200 to light perception 10. No light perception  Pupil  Positive-RAPD+ in affected eye  Negative-No RAPD in affected eye  Zone I. External (limited to bulbar cj, sclera, cornea) II. Ant seg (structures internal to cornea including PC, pars plicata) III. Post seg- all structures post to PC)
Calculating the OTS : variables and raw points Variable Raw points InitialVision NLP 60 LP/HM 70 1/200- 19/200 80 20/200-20/50 90 ≥20/40 100 Rupture -23 Endophthalmitis -17 Perforating Injury -14 Retinal Detachment -11 Afferent pupillary defect -10 Ref : Kuhn F, Maisiak R, Mann L et al.The ocular trauma score Ophtalmol Clin N Am 2002 : 15: 163-165
OTS: Categorization and potential visual acuity outcomes Sum of raw points OTS No PL PL/HM 1/200- 19/200 20/200- 20/50 ≥20/40 0-44 1 74% 15% 7% 3% 1% 45-65 2 27% 26% 18% 15% 15% 66-80 3 2% 11% 15% 31% 41% 81-91 4 1% 2% 3% 22% 73% 92-100 5 0% 1% 1% 5% 94% Ref : Kuhn F, Maisiak R, Mann L et al.The ocular trauma score Ophtalmol Clin N Am 2002 : 15: 163-165
EVALUATION OF THE PATIENT
Evaluation of case of trauma  Proper history  Systemic examination  Visual acuity testing  Thorough Ophthalmic examination using slit lamp and ophthalmoscope, when feasible  In case of chemical injuries, take quick history and give immediate eyewash and treatment. Defer any evaluation till then.
History  Sudden/ gradual changes in vision since the trauma occurred  Pain, diplopia and photophobia  Date and time of incident.  Mechanism of injury  Accidental, intentional or self inflicted  Where it occurred- home, workplace  Use of glasses or protective eyewear  Mechanical trauma with a foreign object  Size and shape  Distance from which it came  Exact location of impact
 Cases of foreign bodies  Composition of FB, contamination  Origin and exact mechanism of impact  Single/multiple  Injuries from animals  Type of animal and nature of injury  Try to locate the animal to test for transmissible diseases  Chemical Injuries  Nature of chemical  Check pH if sample available
 Past ocular history  Pre-existing ocular diseases  Previous ocular surgeries  Visual acuity prior to incidence  Intraocular or periocular appliances  IOL  Scleral buckle  Glaucoma drainage implant  Tetanus immunization  Any treatment taken for the injury in detail
 Systemic Examination  General Condition of patient  Associated head injury, fractures  Any systemic conditions that may need urgent intervention
Location of Injury  Anterior segment  Posterior segment  Adnexa  Orbital structures
Ophthalmic Examination  Record visual acuity on Snellen’s chart  Test each eye individually  Vn with spects  If not available,Vn with pinhole  Near vision  In case of no PL, check with brightest light available (e. g. IDO)  Keep a record  Colour vision  Ophthalmoscopic examination- direct and indirect  Slit lamp examination  Photography  Proper documentation and medico-legal case registration
 Visual field by confrontation test  IOP recording  Deferred until nature of injury is established- open globe/closed  Can be done by Schiotz, Applanation or hand held devices
 Head Posture  Facial Symmetry  Eye alignment  Orbital Fractures- crepitus, infraorbital hypesthesia, restricted EOM  Extra-ocular movements- cranial nerve involvement, entrapment of muscle  Eyebrows, eyelids and eyelashes-  Abrasions, CLWs, marginal and canthal tears including canalicular tears- probing  Ecchymosis, edema  Ptosis, FB, enophthalmos/exophthalmos
 Conjunctiva-  Chemosis, sub-conj. Haemorrhage  Examine fornices for any FB by double eversion  conj FB, abrasions (fluorescein staining), lacerations , emphysema  Cornea-  abrasion- superficial/deep (Fluorescein staining)  Corneal FB- metallic burr/ vegetative matter  Chemical burns, ulceration  Corneal, Corneoscleral tear with/without iris prolapse  Seidel’s test
• Anterior Chamber-  Depth  Gonioscopy- iridodialysis, FB, angle recession  Cells, flare- iritis  Hyphaema , hypopyon  Cortical matter or dislocated lens in AC  Vitreous, FB • Iris- examine before dilating the pupil  Iridodonesis, Iridodialysis  Iris prolapse  Sphincter tears  Traumatic iritis
 Pupil-size, shape and Pupillary Reaction  Traumatic mydriasis  RAPD  D shaped  Lens-  Position- Subluxation/ dislocation of lens  Stability  Clarity- traumatic cataract- rosette shaped cataract  PSC, ant subcapsular cat, Sectoral cataracts  Vossius ring  Capsular integrity
 Vitreous  Pigment (tobacco dusting)  Haemorrhage, IOFB  Weiss ring- indicates PVD  Choroid- choroidal rupture, detachment  Optic Nerve-  Edema, haemorrhage  Note c:d ratio  Avulsion- partial/complete  optic neuritis  Retina- scleral depression is important  Berlin’s edema (commotio retinae)  IOFB  Retinal tears, holes  Retinal dialysis and detachment
INVESTIGATIONS
 Routine haematological investigations  Radiological Imaging-  Plain Radiography- if CT and MRI not available  X-ray orbit AP and Lateral view, PNS  Orbital fractures  IOFB and intraorbital FB
Computed Tomography  Indicated if bone involvement is suspected  Plain/contrast  Axial sections- Globe, MR and LR, medial and lat walls of orbit  Coronal Sections- SR and IR, roof and floor of orbit  Indications  Open globe injuries-  Post seg visualization  Suspected Intraocular and intraorbital FB and haemorrhage  Orbital fractures
Magnetic Resonance Imaging  Indications- soft tissue lesions  To visualise periocular soft tissues  Suspected vascular lesios, intracranial pathology, optic nerve lesions  Non magnetic intraocular or intraorbital FB  Contraindicated in metallic FB, pacemakers and implants
Ultrasonography  Best resolution of post seg (0.1 to 0.01mm)  Extreme caution in c/o open globe injuries- preferably avoided  Indications  Vitreous haemorrhage, PVD  Retinal tears and detachment  Choroidal rupture, suprachoroidal Haemorrhage  Scleral rupture  To visualize Lacrimal gland, EOM, soft tissues, FB
MANAGEMENT
First- Aid  Thorough eyewash- FB , chemical injuries  Cleaning and dressing of the wounds  Do Not give pressure on the eyeball in cases of globe rupture  Apply a shield in case of open globe injuries  Tetanus immunisation  Systemic Analgesics and antibiotics
 Closed globe Injuries  Eyelid injuries  Anterior segment  Posterior segment  Orbital trauma  Open globe injuries  Globe rupture  Lacerations  IOFB
Black Eye  Blunt truma to eye  Massive lid edema, ecchymosis  marked chemosis  Fundus- may show Berlin’s edema  USG B scan  X-ray orbit AP lat view  M/t-  analgesics-anti- inflammatory,  localAntibiotic e/d  Close follow up
Lid Injuries  Commonly associated with polytrauma  Consider patients systemic status before deciding further management  Examination  Examine thoroughly the lids, globe, adnexal tissue, orbit and face  Extent of wound- involvement of orbital septum, muscle, lid margin, canaliculus, medial and lateral canthal injuries  See for tissue loss  Rule out orbital fractures  Look for any foreign bodies in wound  Handle gently
 Principles ofWound Repair  Re-establish the integrity of basic lid parts- ant. Lamella, post lamella, levator, canaliculi and canthal tendons  Identify landmarks and reattach them- wound angles, apex of skin flaps, brow hairline  Do not incorporate orbital septum in the repair  Can be usually done under LA  Sutures-  6-0 polyprolene, nylon , silk  Can use 6-0 polyglycolic acid in young pts  Skin sutures removed after 5-7 days  Major lid reconstructive procedures to be done after 3-6 months
 Non- marginal Lid Lacerations  Subcutaneous closure  Use 6- 0/5-0 Polyglactic acid (vicryl) suture  For suturing of deeper tissue and to anchor it to the periosteum  Not necessary to suture the orbital septum  Tissue loss- consider skin grafts/ flaps
 Marginal Eyelid Lacerations  Clean, anaesthetize and inspect the wound  Freshen edges, separate ant and post lamella by blunt dissection  Tarsus approximated by 5-0Vicryl suture  Pass the needle through partial thickness 2mm from lacerated edge and exit at mid depth  Minimum 2-3 sutures passed and left untied  Pass 5-0 silk suture at level of meibomian glands vertical mattress fashion  Tie both the sutures now  Skin closure with 7-0 Nylon or vicryl and incorporate silk suture ends in it keeping the knot away from cornea
 Canalicular Lacerations-  Lacerations near medial canthus- do probing and check if any part is exposed  Management-  Monocanalicular stent- for external 2/3rds of one canaliculus  Donut stent-silicone bicanalicular stent wih a pigtail probe  Crawford stent
 Post-operative Care  Keep wound clean and dry  Ice packs to reduce edema  Pressure patching- upto 1 week- avoid in children, open globe injury repair, one eyed pts  Antibiotic eye ointment,TDS for 1 week and systemic antibiotics  Skin sutures removed on days 5-7  Margin sutures left for 2 weeks, stents for 3-6 months  Complications  Scarring  Cicatricial entropion/ectropion  Watering  Exposure keratopathy  Traumatic ptosis
Traumatic Sub-Conjunctival Haemorrhage  Traumatic  Rule out causes of Spontaneous SCH-  Valsalva maneuvers- coughing, sneezing, vomiting, wt lifting  Acute bact/viral conjunctivitis  Systemic HTN , anticoagulants  M/t- rule out any other ocular injuries  Wait and watch  Lubricating and antibiotic eyedrops  Oral vitaminC
Corneal Abrasion  MC form of ocular trauma  Causes- f/b, rubbing, fingernail injury, thrown object, chemical exposure  Presentation- intense pain, redness, photophobia, DOV  Clinical Features-  Lid edema  CC+ CCC+  Cr epi defect  Fluorescien staining  Associated keratitis in contact lens users/tree branch injury  See for sub-tarsal FB in linear abrasions
 Treatment-  Debride any loose epithelium with a wet cotton swab/ sharp blade  Removal of any FB in fornices and over cornea  Broad spectrum antibiotics, tear substitutes, cycloplegics  Patching of eye- controversial  Avoid in cases of vegetative trauma, associated keratitis  Re-examine patient after 24 hours
Corneal Foreign Body  MC seen in workplaces- grinding, drilling, hammering, welding, also while driving  Proper history  Record visual acuity  Ocular Examination-  Rule out IOFB and deeper injury  FB in fornices  Extent of FB in cornea  Seidel’s test  Iritis,AC cells, flare  Cataractous changes in lens  Dilated fundus for IOFB
Treatment • Superficial- remove with cotton swab • Deep- 26 no needle • Metallic FB- remove the rust ring •Approach the cornea tangentially •Antibiotic ointment, cycloplegic if required, patch the eye for 6 hours •Follow up after 24 hours •Use of dark goggle •Very deep FB- ideal to remove under microscope as suture may be needed if perforation occurs •Inform patient abt developmet of corneal opacity •Use of protective eyewear
Traumatic Mydriasis  Frequent complication of ocular trauma  Cause-  injury to iris sphincter and dilator muscles, iris nerves and ciliary body  Leads to dilatation of pupil and paralysis of accomodation  Clinical Features  Dull aching pain  watering, photophobia, blurred vision  ocular fatigue  Treatment  Pilocarpine e/d  Tinted contact lenses  Surgical repair
Hyphema  Blood accumulation in AC  2/3rd cases in closed globe injuries and 1/3rd in open globe injuries  Clinical Features  Symptoms- pain, photophobia, reducedV/A  RBCs and proteinaceous material in AC  Whole AC may be filled with clot  Corneal blood staining  IOP- variable  High chances of rebleeding after 3-5 days
 Management  USG B scan- to rule out post seg involvement  Topical Prednisolone acetate 1 % e/d- frequency depends on extent of hyphema  Cycloplegics  Anti glaucoma medications- topical and systemic  Wear eye shield  Propped up position and bed rest  Warning signs of rebleeding explained to pt  Daily follow up
 Surgical Intervention  AC wash with/ without trabeculectomy  Small gauge bimanual vitrectomy  Avoid forceful and vigorous manipulation  Indications  Corneal blood staining  Total hyphema with IOP> 50mm Hg > 5days  Unresolved after 9 days of t/t
 Complications  Corneal blood staining  Peripheral anterior synechiae  Ischemic optic neuropathy  Optic atrophy, Decreased vision and visual field defects  Amblyopia in children d/t corneal blood staining
TRAUMATIC CATARACT  Seen in contusive eye trauma immediately or after years  Reported in 11 % eyes with closed globe injuries  Mechanism- coup and contrecoup  Cinical Features  Associated with injuries to other structures  Phacodonesis  Capsular tears  Vitreous prolapse  Most commonly ant and post subcapsular cataracts- rosette shaped  Predisposition to progress to mature cataracts
 Management  USG B scan- to rule out retinal detachment,tear, IOFB  In early stages, refraction  For advanced cataracts, phacoemulsification and IOL implantation  Use of capsular hooks and CTR in c/o capsular instability  Pars plana vitrectomy and lensectomy  Preferable to do Posterior capsulotomy and ant vitrectomy in children to avoid PCO  Early surgery will prevent amblyopia in children
Traumatic Luxation of Lens  Lens drawn away from the site of zonular rupture  AC- asymmetric  Lens may dislocate in AC, posterorly or extruded  Symptoms- diminution of vision, monocular diplopia,  Management  Spectacles/contact lenses  Miotics  Mild- Capsular hooks/CTR with phacoemulsification and PCIOL  Severe- ICCE with ACIOL  Severe with vitreous prolapse- PPV + lensectomy  Lens in AC- anti- inflammatory, anti- glaucoma, DO NOT DILATE- lens extraction with ACIOL or SFIOL  Lens in vitreous cavity- PPV with phacofragmentation
Commotio Retinae  MC retinal manifestation of contusive injury  Mechanism- damage to photoreceptor outer segment and RPE- coup and countercoup injury  Clinical Presentation  Confluent geographic areas of retinal whitening  In mid-perphery  Involving macula- Berlin’s edema  A/w acute vision loss if macula involved  Management  Rule out associated injuries  Wait and watch
Traumatic Vitreous Haemorrhage  Clinical Features  sudden, punctate or web like floaters  Decreased visual acuity  Seeing red  Diagnosis  Ophthalmoscopic examination  USG B scan-  Mild to moderateVH-mobile opacities  MarkedVH- dense echoes  Positional shifting of Haemorrhage differentiates from RD  Management  Closed globe injury withVH, no RD/break-  bed rest, head elevation  Re-examination within 2 weeks for resolution/RD  Non-resolvingVH- Persisting for 2-3 months-Vitrectomy  Associated with RD- early vitrectony  Complications  Secondary open angle glaucoma  Hemosiderosis  PVR,Tractional RD  Synchysis scintillans
Choroidal rupture  Traumatic break in RPE, Bruch’s membrane, and underlying choroid  Classically crescent shaped with tapered ends concentric to Optic nerve  Direct/indirect – may involve macula  Immediate -loss of vision- involvement of macula or serous detachment, retinal edema, haemorrhage  Late- ERM, CNVM, serous RD  Management  Regular fundus examination 6 monthly- to detect CNVM  For CNVM- observation, photocoagulation, photodynamic therapy, anti-VEGF agents
Suprachoroidal Haemorrhage  Haemorrhgic choroidal detachment a/w accumulation of blood in potential space between choroid and sclera  Rupture of long/short post ciliary arteries r ciliary body vessels  a/w penetrating ocular injuries  Presentation-  Shallow/flatAC, with/without expulsion of intraocular contents  Pain, raised IOP  Fundus- dark, dome shped elevation of retina, choroid- loss of red reflex, apex towards post pole  USG- non- mobile, flat/dome shaped echo dense opacities in suprachoroidal space  Management  A/w closed globe injury- observe  Drainage, if indicated- on day 7-14  A/ w open globe- early surgical intervention
Traumatic Retinal Detachment Various predisposing conditions which have a common final outcome i. e. retinal detachment are  Retinal Dialysis  Giant RetinalTears  Horseshoe tears  Necrotic Retinal Breaks  Vitreous base avulsion  Traumatic posterior vitreous detachment  Pars plana tears
Retinal Dialysis  Disinsertion of the retina from non-pigmented pars plana epithelium at the ora serrata  Retina remains attached to vitreous base  MC location Inferotemporal quadrant and in traumatic cases- superonasal  May remain undiagnosed for long periods d/t minimal symptoms
Giant Retinal Tears  Extends from min 90 degrees/ 3 clock hours  Typically located in inferotemporal and superonasal quadrants  a/w posterior vitreous detachment
Horseshoe Tears  Areas of strong vitreoretinal adhesion cause retinal break during traumatic/spontaneous PVD  They take shape of a horseshoe  Globe deformations and torsion leading to PVD and fluid collects subsequently in the subretinal space
Necrotic Retinal Breaks  Seen posterior to ora serrata  Direct contusive damage, retinal vascular damage and retinal capillary necrosis leads to weakened retina and irregularly shaped retinal breaks  Detachment tends to form within 24 hours
Vitreous Base Avulsion  Occurs commonly after blunt trauma  Associated with pars plana tears, retinal dialysis, retinal tears  Bucket handle appearance- stripe of translucent vitreous over the retina  May be asymptomatic, but should search for associated conditions
Treatment  Wait and watch  Prophylactic laser retinopexy/ trans-scleral cryopexy- peripheral retinal breaks  Aim of surgery- close all retinal breaks and relieve vitreoretinal traction  Surgical techniques- pneumatic retinopexy, scleral buckling and/or PPV  Giant retinal tears- PFC stabilization, lensectomy, , silicon oil tamponade  RD with pars plana tears/ retinal dialysis- scleral buckling with trans-scleral cryotherapy or PPV, air-fluid exchange, internal drainage of SRF and endolaser photocoagulation
Traumatic Optic Neuropathy  Intracanalicular part is most vulnerable  Mechanism of damage to optic nerve  Direct deformation of skull and optic canal  Shearing of ON microvasculature  Tearing of nerve axons  Contusion against optic canal  Presentation  Profound visual loss, loss of centralVA  Visual field defects  RAPD  Colour vision defects  Management  CT gold standard  Observation  High dose corticosteroids -IV methylprednisolone 30 mg/kg f/b 15 mg/kg 6 hourly  Optic canal decompression
Orbital Trauma  Orbital injury can be contusive/ penetrating  Evaluation-  Periorbital oedema, lacerations, FB  Ptosis- edema, haemorrhage, neurogenic  Crepitus/bony discontinuity- orbital fractures  Enophthalmos-large orbital #  Exophthalmos- edema, haemorrhage, bony fragments, air  EOM- muscle entrapment, IR mostly involved  Check Sensations- infraorbital nerve distribution  Nasal passages- epistaxis, CSF rhinorrhea
 Blowout Fractures  Expansion of orbital volume due to fracture of the thin orbital walls into adjacent paranasal sinuses  ‘Hydraulic theory’ and ‘buckling theory’  Axial and Coronal CT scan  Management  Systemic oral antibiotics, nasal decongestants, ice packs  Surgery indicated-  Entrapment of IR or perimuscular tissue with diplopia  Significant enophthalmos upto 7-10 days  High risk injuries for enophthalmos  Large floor/medial wall #  Combined medial wall and floor #
 Surgery-  MedialWall-Floor / transcaruncular incision  Orbital floor  approached through transconjunctival/ sunciliary incision  Entrapped tissues are released  Orbital implant- nylon sheets, polyethylene, teflon, bone
Open Globe Injuries  Globe rupture- full thickness eyewall injury caused by blunt trauma  Laceration- full thickness eyewall wound caused by sharp object  Corneal laceration  Corneoscleral laceration  Scleral laceration
 Ophthalmic Examination  360 degreee sub-conjunctival haemorrhage  ‘Jelly Roll’ chemosis  Relative asymmetry in AC depth-  shallow in injuries ant to ciliary body  deep – post seg involvement  Transillumination defects in iris- path of projectile injuries  Violation of ant capsule, focal cataract  Seidel test  Rule outVH, IOFB, RD by dilated examination
Management  Avoid manipulation of eye, put a protective shield over the injured eye  Timing of the surgery depends upon systemic condition of the patient  Repair can be performed under Peribulbar anaesthesia in adults and under GA in children  Start systemic antibiotics- IV aminoglycosides and 3rd generation cephalosporins
Surgery  Examination of eye under microscope and devise a surgical strategy  Goals  Close the globe with minimal manipulation  Reposit/ excise exposed intraocular contents  Explore the globe for unrecognized injuries  Decrease the risk of endophthalmitis and maximize chances of functional recovery by restoring ocular integrity
Corneal Lacerations  Small, self-sealing clean corneal lacerations without iris incarceration- cyanoacrylate glue application  Large lacerations  Limbal paracentesis site created  Injection of viscoelastic substance in AC  Iris repositioned, if necrotic abscission required  Thorough wash with BSS  Sutures taken with 10-0 nylon, start with central suture  Wound divided in two halves at the pass of each suture  75% and 90% depth of suture pass optimal for healing  Depth equal on either side, adequate tension  Longer passes- less astigmatism  Adequate sutures in periphery, less near visual axis  Sutures rotated and buried once the wound is stabilized  Subconj inj antibiotic and steroid is given, eye patched and shield placed
Corneoscleral Laceration  Larger wound with higher incidence of uveal prolapse or incarceration  Primarily stabilize the limbus by a 9-0 nylon suture  Repair in anterior to posterior direction
Scleral Laceration  Identify the posterior extent of the laceration  Dissect overlying conjunctiva andTenon’s capsule  Sutures taken with 8-0 or 9-0 nylon  Initially place one or two central sutures for easier repositioning of uveal tissue  Suture pass should be atleast 50% depth, full thickness passes avoided  Interrupted sutures preferred, ends are cut and rotated if possible
 Rectus muscle laceration- muscle is secured with double armed 6-0 vicryl, disinserted from globe, and resutured after wound closure to its original attachment  Posterior scleral lacerations  360 degree conjuctival peritomy  Isolate all recti on muscle hhoks and secure with loop of 2-0 braided polyester suture  Suturing performed, most post part may be leftto heal by secondary intention  Tissue loss- scleral or corneal patch graft  Conjunctiva closed with 6-0 vicryl
Pre-op Post op
Ruptured Globe Repair  Exploratory surgery  360 degree conjunctival peritomy  Bipolar cautery for haemostasis  Wound closure performed as described earlier
Post-operative Management  Thourough clinical examination  Topical antibiotics, steroids, cycloplegics, tear substitutes  IOP lowering agents in case it is elevated  Eye shielded, avoid strenuous activities  Continue systemic antibiotics, shift to oral  Use of soft bandaged contact lenses  VR consultation in cases of  IOFB  Endophthalmitis  RD,VH  Posterior scleral rupture/ laceration  Choroidal detachment, dislocated lens  Frequent follow-ups  Suture removal after 4-6 weeks
Complications and Outcomes  Poor prognostic signs-  Initial visual acuity at presentation  Length and width of laceration  Lacerations of recti  Involvement of lens  VH, RD  Endophthalmitis, sympathetic ophthalmia  Irregular astigmatism- Rigid gas permeable contact lenses can be used
Intraocular Foreign Bodies  Penetrating ocular trauma with IOFB is a challenging situation for an ophthalmologist  Diagnosis requires thorough history, examination and proper imaging
 Ophthalmic examination  Subconj haemorrhage, iris transillumination defects  Hyphema, focal lens opacity  Corneal/scleral laceration  Violation of ant or post lens capsule  VH, intra/ sub-retinal haemorrhage  Relative hypotony  Visible FB  Gonioscopy- FB in angle  Mainstay in imaging- USG and CT, preferably helical CT with 1mm cuts
Management  Anterior chamber FB  Entry wound in cornea is closed as described earlier  Limbal paracentesis/ clear corneal incision made away from the wound  FB directly visualised, use of surgical gonioscopy lens (Koeppe’s lens)  Grasped with forceps and removed, may need bimanual manipulation  Metallic FB – use of intraocular magnet
 Intralenticular FB-  can be managed by lens extraction by phacomulsification and forceps extracion of FB  Posterior segment FB  Immediate removal is advocated  Stabilization of the wound  Pars plana lens extraction  Stabilization and repair of retina  Forceps/ magnetic removal of FB  Scleral buckling, intravitreal injections
Delayed Complications of ocular injury  Traumatic Iritis  Traumatic cataract  Delayed trauma-related glaucoma  Angle recession glaucoma  Vitreous haemorrhage- induced glaucoma  Lens- induced glaucoma  Retinal Detachment  Metallosis bulbi- siderosis bulbi, chalcosis  Sympathetic ophthalmia  Choroidal Neovascularization  Traumatic endophthalmitis
Sympathetic Ophthalmia  Bilateral granulomatous uveitis  MC following open globe injury (incidence 0.2 to 0.5%), may also occur after intraocular surgery  Pathophysiology-  Traumatic injury- uveal antigens are exposed- autoimmune response  Exciting/injured eye and sympathizing/ normal eye both become inflamed  A/w HLA-A 11 is shown  Onset- 2 weeks to 6 months after injury, mostly within 3 months
 Clinical Features  Mild pain, photophobia, DOV  Mutton fat keratic precipitates  Granulomatous panuveitis with prominent vitritis  Choroidal lesions- multifocal, placoid, cream colored- Dalen Fuch’s nodules  Optic nerve hyperemia, swelling  FA- multiple hyperfluorescent sites leak in late phase  Management  Prevention- enucleation of severely injured eye  T/t-  High dose steroids with tapering  Cyclosporine, azathioprine, chlorambucil, methotrexate
Traumatic Endophthalmitis  Incidence 4-7%  Risk factors- IOFB, lens capsule violation, contamination, delayed primary repair  Presentation- pain, hypopyon, membranous vitreous opacities  Diagnosis- clinical  Organisms- Staph. Epidermidis, Bacillus cereus, Streptococcus  Treatment-  Vitreous aspiration for culture with intravitreal inj of antibiotics  PPV with intravitreal inj of antibiotics
Non- Mechanical Eye Injuries  Chemical Injuries  Thermal Injuries  Ultrasonic Injuries  Electrical Injuries  Radiational Injuries
Chemical Injuries  True ocular emergencies, every second counts  Immediate irrigation is vital  Check pH in cul de sac if possible.  Type of chemical  Alkali- most severe damage- rapid penetration- saponification of cell membranes, denaturation of collagen  Acids- less damage- hydrogen ion precipitates proteins and prevents penetration
Roper- Hall modification of Hughes classification
 After thorough irrigation, record visual acuity, IOP  Lids ,lashes- crystallized chemicals  Upper and lower fornix- swipe with cotton swab  Size of corneal epi defect, limbal ischemia in clock hours  AC reaction
 Management  Copious irrigation underTA with liter bags of saline with monitoring of pH till pH neutralizes  Perform in a lying down position  Use retractors  Antibiotic eye ointments, cycloplegic, tear substitutes  Topical steroids with tapering  10 % ascorbate and 10% citrate e/d 2hrly  OralVit C 500mg  Oral Doxycycline 50-100mg BD- collagenase inhibitor  Control of raised IOP- topical beta blockers, alpha agonists,CA inhibitors  Monitor daily  SurgicalT/t- temporary tarsorrhaphy, corneal glue, patch graft
Thermal Injuries  Hyperthermal Injuries  Flame burns, contact burns  Clinical Presentations  Conj hyperemia, chemosis  Corneal superficial /deep burns- corneal opacification, sloughing  Healing- leucoma formation  Bullous keratitis, ectasia, staphyloma, symblepharon  Scleral involvement- uveal prolapse, uveitis, panophthalmitis
 Treatment  Clean with saline  Antibiotic cream  Full thickness burns of lid- grafting  Topical – atropine, antibiotics, lubricating e/d, steroids  Glass rod passed in fornices  Conj transposition flap, amniotic membrane graft, limbal cell transplant  PK or LK for leucomatous corneal opacity later stage
 Hypothermal Injuries  Surgical Hypothermia-Cardiovascular/ neurosurgery  Accidental hypothermia  Cryosurgery  Clinical lesions  Conj congestion, edema  Muscle, tendons- edema and haemorrhage  Ciliary body- reduced aqueous formation  Adhesive chorioretinal traction, vitreous iceballs
Electrical Injuries  Point of entry and exit  Clinical Features-  Lid burns- entry wound  Corneal interstitial opacities  Iritis, miosis, spasm of accomodation  Electric cataract  Retinal edema, papilloedema, RD , chorioretinitis  Optic neuritis
Radiational Injuries  Ionizing radiations- X rays, beta rays  Loss of lashes, entropion, ectropion  Conj scarring  Cataract  UV radiations  Damage to corneal epithelium  Cataract formation  Visible radiation  Thermal injuries  Sun gazing l/t damage to macula  Infrared radiation- Glassblower’s cataract  Welding arc injuries
Prevention  Patient education  Use of protective eyewear at workplaces and in sports activities  Use of helmet while riding two wheelers  Parent education to avoid eye injuries with household items in children  Safety norms should be introduced in workplaces regarding protection of eyes
Take Home Message…  Immediate treatment is directed at preventing further injury or vision loss  Never think of the eye in isolation, always compare both eyes  Always record visual acuity as it has important medicolegal implications  A visual acuity of 6/6 does not necessarily exclude a serious eye injury  Beware of the unilateral red eye as it is rarely ‘just’ conjunctivitis  Documentation  Use of protective eyewear
References  Indian J Ophthalmol. 2013 Oct; 61(10): 539–540 PMCID: PMC3853447 Ocular trauma, an evolving sub specialty Sundaram Natarajan  Ngrel AD, Thylefors B. The global impact of eye injuries [J] Ophthalmic Epidemiol. 1998;5:143–69. PubMed  Ocular trauma by James T. Banta  Clinical Diagnosis and management of ocular trauma by Garg, Moreno, Shukla et al
Ocular trauma

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Ocular trauma

  • 1.
    OCULAR TRAUMA ANDBASIC MANAGEMENT PRINCIPLES By Dr. Amreen Deshmukh Under Guidance of Dr. K. G.Choudhary Sir
  • 2.
    Outline  Introduction  Epidemiology Classification  Evaluation  General principles  Management of individual conditions  Complications  Prevention  Conclusion
  • 3.
    Introduction  It issaid that “ Eyes are window to the soul and to the outer world.”  Ocular trauma is a major cause of preventable monocular blindness and visual impairment in the world, especially in the developing countries  Ocular trauma and resultant loss of vision leads to psychological, economical and professional crippling of the patient.
  • 4.
    Epidemiology  Bimodal agedistribution: children and young adults;>70 yrs of age  M/F: 3-5x  Lifetime prevalence 20%: 3x recurrence risk  workplace, sports, falls(elderly)  PUBLIC HEALTH ISSUE
  • 5.
     TheWHO Programmefor the Prevention of Blindness, suggests that annually  55 million eye injuries restricting activities more than one day  750,000 cases will require hospitalization  200,000 open-globe injuries  approximately 1.6 million blind from injuries  2.3 million people with bilateral low vision  19 million with unilateral blindness or low vision.
  • 6.
    Classification of OcularTrauma  The Birmingham EyeTraumaTerminology System (BETTS) devised a classification for ocular trauma which is accepted worldwide.  It is unambiguous, consistent and simple.
  • 7.
    Eye Injury ClosedGlobe Contusion Lamellar Laceration Open Globe Rupture Blunttrauma Laceration Penetrating Injury IOFB Perforating Injury BETTS Classification
  • 10.
    Open Globe Injury Classification Type 1. Rupture 2. Penetrating 3. Intraocular 4. Perforating 5. Mixed  Grade- visual acuity 1. ≥20/40 2. 20/50 to 20/100 3. 19/100 to 5/200 4. 4/200 to light perception 5. No light perception  Pupil  Positive-RAPD+ in affected eye  Negative-No RAPD in affected eye  Zone I. I- Isolated to cornea (Including the corneoscleral limbus II. II- Corneoscleral limbus to a point 5mm posterior into the sclera III. III- Posterior to anterior 5mm of sclera
  • 11.
    Closed Globe Injury Classification Type 1. Contusion 2. Lamellar laceration 3. Superficial foreign body 4. Mixed  Grade- visual acuity 6. ≥20/40 7. 20/50 to 20/100 8. 19/100 to 5/200 9. 4/200 to light perception 10. No light perception  Pupil  Positive-RAPD+ in affected eye  Negative-No RAPD in affected eye  Zone I. External (limited to bulbar cj, sclera, cornea) II. Ant seg (structures internal to cornea including PC, pars plicata) III. Post seg- all structures post to PC)
  • 12.
    Calculating the OTS: variables and raw points Variable Raw points InitialVision NLP 60 LP/HM 70 1/200- 19/200 80 20/200-20/50 90 ≥20/40 100 Rupture -23 Endophthalmitis -17 Perforating Injury -14 Retinal Detachment -11 Afferent pupillary defect -10 Ref : Kuhn F, Maisiak R, Mann L et al.The ocular trauma score Ophtalmol Clin N Am 2002 : 15: 163-165
  • 13.
    OTS: Categorization andpotential visual acuity outcomes Sum of raw points OTS No PL PL/HM 1/200- 19/200 20/200- 20/50 ≥20/40 0-44 1 74% 15% 7% 3% 1% 45-65 2 27% 26% 18% 15% 15% 66-80 3 2% 11% 15% 31% 41% 81-91 4 1% 2% 3% 22% 73% 92-100 5 0% 1% 1% 5% 94% Ref : Kuhn F, Maisiak R, Mann L et al.The ocular trauma score Ophtalmol Clin N Am 2002 : 15: 163-165
  • 14.
  • 15.
    Evaluation of caseof trauma  Proper history  Systemic examination  Visual acuity testing  Thorough Ophthalmic examination using slit lamp and ophthalmoscope, when feasible  In case of chemical injuries, take quick history and give immediate eyewash and treatment. Defer any evaluation till then.
  • 16.
    History  Sudden/ gradualchanges in vision since the trauma occurred  Pain, diplopia and photophobia  Date and time of incident.  Mechanism of injury  Accidental, intentional or self inflicted  Where it occurred- home, workplace  Use of glasses or protective eyewear  Mechanical trauma with a foreign object  Size and shape  Distance from which it came  Exact location of impact
  • 17.
     Cases offoreign bodies  Composition of FB, contamination  Origin and exact mechanism of impact  Single/multiple  Injuries from animals  Type of animal and nature of injury  Try to locate the animal to test for transmissible diseases  Chemical Injuries  Nature of chemical  Check pH if sample available
  • 18.
     Past ocularhistory  Pre-existing ocular diseases  Previous ocular surgeries  Visual acuity prior to incidence  Intraocular or periocular appliances  IOL  Scleral buckle  Glaucoma drainage implant  Tetanus immunization  Any treatment taken for the injury in detail
  • 19.
     Systemic Examination General Condition of patient  Associated head injury, fractures  Any systemic conditions that may need urgent intervention
  • 20.
    Location of Injury Anterior segment  Posterior segment  Adnexa  Orbital structures
  • 21.
    Ophthalmic Examination  Recordvisual acuity on Snellen’s chart  Test each eye individually  Vn with spects  If not available,Vn with pinhole  Near vision  In case of no PL, check with brightest light available (e. g. IDO)  Keep a record  Colour vision  Ophthalmoscopic examination- direct and indirect  Slit lamp examination  Photography  Proper documentation and medico-legal case registration
  • 22.
     Visual fieldby confrontation test  IOP recording  Deferred until nature of injury is established- open globe/closed  Can be done by Schiotz, Applanation or hand held devices
  • 23.
     Head Posture Facial Symmetry  Eye alignment  Orbital Fractures- crepitus, infraorbital hypesthesia, restricted EOM  Extra-ocular movements- cranial nerve involvement, entrapment of muscle  Eyebrows, eyelids and eyelashes-  Abrasions, CLWs, marginal and canthal tears including canalicular tears- probing  Ecchymosis, edema  Ptosis, FB, enophthalmos/exophthalmos
  • 24.
     Conjunctiva-  Chemosis,sub-conj. Haemorrhage  Examine fornices for any FB by double eversion  conj FB, abrasions (fluorescein staining), lacerations , emphysema  Cornea-  abrasion- superficial/deep (Fluorescein staining)  Corneal FB- metallic burr/ vegetative matter  Chemical burns, ulceration  Corneal, Corneoscleral tear with/without iris prolapse  Seidel’s test
  • 25.
    • Anterior Chamber- Depth  Gonioscopy- iridodialysis, FB, angle recession  Cells, flare- iritis  Hyphaema , hypopyon  Cortical matter or dislocated lens in AC  Vitreous, FB • Iris- examine before dilating the pupil  Iridodonesis, Iridodialysis  Iris prolapse  Sphincter tears  Traumatic iritis
  • 26.
     Pupil-size, shapeand Pupillary Reaction  Traumatic mydriasis  RAPD  D shaped  Lens-  Position- Subluxation/ dislocation of lens  Stability  Clarity- traumatic cataract- rosette shaped cataract  PSC, ant subcapsular cat, Sectoral cataracts  Vossius ring  Capsular integrity
  • 27.
     Vitreous  Pigment(tobacco dusting)  Haemorrhage, IOFB  Weiss ring- indicates PVD  Choroid- choroidal rupture, detachment  Optic Nerve-  Edema, haemorrhage  Note c:d ratio  Avulsion- partial/complete  optic neuritis  Retina- scleral depression is important  Berlin’s edema (commotio retinae)  IOFB  Retinal tears, holes  Retinal dialysis and detachment
  • 28.
  • 29.
     Routine haematologicalinvestigations  Radiological Imaging-  Plain Radiography- if CT and MRI not available  X-ray orbit AP and Lateral view, PNS  Orbital fractures  IOFB and intraorbital FB
  • 30.
    Computed Tomography  Indicatedif bone involvement is suspected  Plain/contrast  Axial sections- Globe, MR and LR, medial and lat walls of orbit  Coronal Sections- SR and IR, roof and floor of orbit  Indications  Open globe injuries-  Post seg visualization  Suspected Intraocular and intraorbital FB and haemorrhage  Orbital fractures
  • 31.
    Magnetic Resonance Imaging Indications- soft tissue lesions  To visualise periocular soft tissues  Suspected vascular lesios, intracranial pathology, optic nerve lesions  Non magnetic intraocular or intraorbital FB  Contraindicated in metallic FB, pacemakers and implants
  • 32.
    Ultrasonography  Best resolutionof post seg (0.1 to 0.01mm)  Extreme caution in c/o open globe injuries- preferably avoided  Indications  Vitreous haemorrhage, PVD  Retinal tears and detachment  Choroidal rupture, suprachoroidal Haemorrhage  Scleral rupture  To visualize Lacrimal gland, EOM, soft tissues, FB
  • 33.
  • 34.
    First- Aid  Thorougheyewash- FB , chemical injuries  Cleaning and dressing of the wounds  Do Not give pressure on the eyeball in cases of globe rupture  Apply a shield in case of open globe injuries  Tetanus immunisation  Systemic Analgesics and antibiotics
  • 35.
     Closed globeInjuries  Eyelid injuries  Anterior segment  Posterior segment  Orbital trauma  Open globe injuries  Globe rupture  Lacerations  IOFB
  • 36.
    Black Eye  Blunttruma to eye  Massive lid edema, ecchymosis  marked chemosis  Fundus- may show Berlin’s edema  USG B scan  X-ray orbit AP lat view  M/t-  analgesics-anti- inflammatory,  localAntibiotic e/d  Close follow up
  • 37.
    Lid Injuries  Commonlyassociated with polytrauma  Consider patients systemic status before deciding further management  Examination  Examine thoroughly the lids, globe, adnexal tissue, orbit and face  Extent of wound- involvement of orbital septum, muscle, lid margin, canaliculus, medial and lateral canthal injuries  See for tissue loss  Rule out orbital fractures  Look for any foreign bodies in wound  Handle gently
  • 38.
     Principles ofWoundRepair  Re-establish the integrity of basic lid parts- ant. Lamella, post lamella, levator, canaliculi and canthal tendons  Identify landmarks and reattach them- wound angles, apex of skin flaps, brow hairline  Do not incorporate orbital septum in the repair  Can be usually done under LA  Sutures-  6-0 polyprolene, nylon , silk  Can use 6-0 polyglycolic acid in young pts  Skin sutures removed after 5-7 days  Major lid reconstructive procedures to be done after 3-6 months
  • 39.
     Non- marginalLid Lacerations  Subcutaneous closure  Use 6- 0/5-0 Polyglactic acid (vicryl) suture  For suturing of deeper tissue and to anchor it to the periosteum  Not necessary to suture the orbital septum  Tissue loss- consider skin grafts/ flaps
  • 40.
     Marginal EyelidLacerations  Clean, anaesthetize and inspect the wound  Freshen edges, separate ant and post lamella by blunt dissection  Tarsus approximated by 5-0Vicryl suture  Pass the needle through partial thickness 2mm from lacerated edge and exit at mid depth  Minimum 2-3 sutures passed and left untied  Pass 5-0 silk suture at level of meibomian glands vertical mattress fashion  Tie both the sutures now  Skin closure with 7-0 Nylon or vicryl and incorporate silk suture ends in it keeping the knot away from cornea
  • 41.
     Canalicular Lacerations- Lacerations near medial canthus- do probing and check if any part is exposed  Management-  Monocanalicular stent- for external 2/3rds of one canaliculus  Donut stent-silicone bicanalicular stent wih a pigtail probe  Crawford stent
  • 42.
     Post-operative Care Keep wound clean and dry  Ice packs to reduce edema  Pressure patching- upto 1 week- avoid in children, open globe injury repair, one eyed pts  Antibiotic eye ointment,TDS for 1 week and systemic antibiotics  Skin sutures removed on days 5-7  Margin sutures left for 2 weeks, stents for 3-6 months  Complications  Scarring  Cicatricial entropion/ectropion  Watering  Exposure keratopathy  Traumatic ptosis
  • 44.
    Traumatic Sub-Conjunctival Haemorrhage  Traumatic Rule out causes of Spontaneous SCH-  Valsalva maneuvers- coughing, sneezing, vomiting, wt lifting  Acute bact/viral conjunctivitis  Systemic HTN , anticoagulants  M/t- rule out any other ocular injuries  Wait and watch  Lubricating and antibiotic eyedrops  Oral vitaminC
  • 45.
    Corneal Abrasion  MCform of ocular trauma  Causes- f/b, rubbing, fingernail injury, thrown object, chemical exposure  Presentation- intense pain, redness, photophobia, DOV  Clinical Features-  Lid edema  CC+ CCC+  Cr epi defect  Fluorescien staining  Associated keratitis in contact lens users/tree branch injury  See for sub-tarsal FB in linear abrasions
  • 46.
     Treatment-  Debrideany loose epithelium with a wet cotton swab/ sharp blade  Removal of any FB in fornices and over cornea  Broad spectrum antibiotics, tear substitutes, cycloplegics  Patching of eye- controversial  Avoid in cases of vegetative trauma, associated keratitis  Re-examine patient after 24 hours
  • 47.
    Corneal Foreign Body MC seen in workplaces- grinding, drilling, hammering, welding, also while driving  Proper history  Record visual acuity  Ocular Examination-  Rule out IOFB and deeper injury  FB in fornices  Extent of FB in cornea  Seidel’s test  Iritis,AC cells, flare  Cataractous changes in lens  Dilated fundus for IOFB
  • 48.
    Treatment • Superficial- removewith cotton swab • Deep- 26 no needle • Metallic FB- remove the rust ring •Approach the cornea tangentially •Antibiotic ointment, cycloplegic if required, patch the eye for 6 hours •Follow up after 24 hours •Use of dark goggle •Very deep FB- ideal to remove under microscope as suture may be needed if perforation occurs •Inform patient abt developmet of corneal opacity •Use of protective eyewear
  • 49.
    Traumatic Mydriasis  Frequentcomplication of ocular trauma  Cause-  injury to iris sphincter and dilator muscles, iris nerves and ciliary body  Leads to dilatation of pupil and paralysis of accomodation  Clinical Features  Dull aching pain  watering, photophobia, blurred vision  ocular fatigue  Treatment  Pilocarpine e/d  Tinted contact lenses  Surgical repair
  • 50.
    Hyphema  Blood accumulationin AC  2/3rd cases in closed globe injuries and 1/3rd in open globe injuries  Clinical Features  Symptoms- pain, photophobia, reducedV/A  RBCs and proteinaceous material in AC  Whole AC may be filled with clot  Corneal blood staining  IOP- variable  High chances of rebleeding after 3-5 days
  • 51.
     Management  USGB scan- to rule out post seg involvement  Topical Prednisolone acetate 1 % e/d- frequency depends on extent of hyphema  Cycloplegics  Anti glaucoma medications- topical and systemic  Wear eye shield  Propped up position and bed rest  Warning signs of rebleeding explained to pt  Daily follow up
  • 52.
     Surgical Intervention AC wash with/ without trabeculectomy  Small gauge bimanual vitrectomy  Avoid forceful and vigorous manipulation  Indications  Corneal blood staining  Total hyphema with IOP> 50mm Hg > 5days  Unresolved after 9 days of t/t
  • 53.
     Complications  Cornealblood staining  Peripheral anterior synechiae  Ischemic optic neuropathy  Optic atrophy, Decreased vision and visual field defects  Amblyopia in children d/t corneal blood staining
  • 54.
    TRAUMATIC CATARACT  Seenin contusive eye trauma immediately or after years  Reported in 11 % eyes with closed globe injuries  Mechanism- coup and contrecoup  Cinical Features  Associated with injuries to other structures  Phacodonesis  Capsular tears  Vitreous prolapse  Most commonly ant and post subcapsular cataracts- rosette shaped  Predisposition to progress to mature cataracts
  • 55.
     Management  USGB scan- to rule out retinal detachment,tear, IOFB  In early stages, refraction  For advanced cataracts, phacoemulsification and IOL implantation  Use of capsular hooks and CTR in c/o capsular instability  Pars plana vitrectomy and lensectomy  Preferable to do Posterior capsulotomy and ant vitrectomy in children to avoid PCO  Early surgery will prevent amblyopia in children
  • 56.
    Traumatic Luxation ofLens  Lens drawn away from the site of zonular rupture  AC- asymmetric  Lens may dislocate in AC, posterorly or extruded  Symptoms- diminution of vision, monocular diplopia,  Management  Spectacles/contact lenses  Miotics  Mild- Capsular hooks/CTR with phacoemulsification and PCIOL  Severe- ICCE with ACIOL  Severe with vitreous prolapse- PPV + lensectomy  Lens in AC- anti- inflammatory, anti- glaucoma, DO NOT DILATE- lens extraction with ACIOL or SFIOL  Lens in vitreous cavity- PPV with phacofragmentation
  • 58.
    Commotio Retinae  MCretinal manifestation of contusive injury  Mechanism- damage to photoreceptor outer segment and RPE- coup and countercoup injury  Clinical Presentation  Confluent geographic areas of retinal whitening  In mid-perphery  Involving macula- Berlin’s edema  A/w acute vision loss if macula involved  Management  Rule out associated injuries  Wait and watch
  • 59.
    Traumatic Vitreous Haemorrhage Clinical Features  sudden, punctate or web like floaters  Decreased visual acuity  Seeing red  Diagnosis  Ophthalmoscopic examination  USG B scan-  Mild to moderateVH-mobile opacities  MarkedVH- dense echoes  Positional shifting of Haemorrhage differentiates from RD  Management  Closed globe injury withVH, no RD/break-  bed rest, head elevation  Re-examination within 2 weeks for resolution/RD  Non-resolvingVH- Persisting for 2-3 months-Vitrectomy  Associated with RD- early vitrectony  Complications  Secondary open angle glaucoma  Hemosiderosis  PVR,Tractional RD  Synchysis scintillans
  • 61.
    Choroidal rupture  Traumaticbreak in RPE, Bruch’s membrane, and underlying choroid  Classically crescent shaped with tapered ends concentric to Optic nerve  Direct/indirect – may involve macula  Immediate -loss of vision- involvement of macula or serous detachment, retinal edema, haemorrhage  Late- ERM, CNVM, serous RD  Management  Regular fundus examination 6 monthly- to detect CNVM  For CNVM- observation, photocoagulation, photodynamic therapy, anti-VEGF agents
  • 62.
    Suprachoroidal Haemorrhage  Haemorrhgicchoroidal detachment a/w accumulation of blood in potential space between choroid and sclera  Rupture of long/short post ciliary arteries r ciliary body vessels  a/w penetrating ocular injuries  Presentation-  Shallow/flatAC, with/without expulsion of intraocular contents  Pain, raised IOP  Fundus- dark, dome shped elevation of retina, choroid- loss of red reflex, apex towards post pole  USG- non- mobile, flat/dome shaped echo dense opacities in suprachoroidal space  Management  A/w closed globe injury- observe  Drainage, if indicated- on day 7-14  A/ w open globe- early surgical intervention
  • 63.
    Traumatic Retinal Detachment Variouspredisposing conditions which have a common final outcome i. e. retinal detachment are  Retinal Dialysis  Giant RetinalTears  Horseshoe tears  Necrotic Retinal Breaks  Vitreous base avulsion  Traumatic posterior vitreous detachment  Pars plana tears
  • 64.
    Retinal Dialysis  Disinsertionof the retina from non-pigmented pars plana epithelium at the ora serrata  Retina remains attached to vitreous base  MC location Inferotemporal quadrant and in traumatic cases- superonasal  May remain undiagnosed for long periods d/t minimal symptoms
  • 65.
    Giant Retinal Tears Extends from min 90 degrees/ 3 clock hours  Typically located in inferotemporal and superonasal quadrants  a/w posterior vitreous detachment
  • 66.
    Horseshoe Tears  Areasof strong vitreoretinal adhesion cause retinal break during traumatic/spontaneous PVD  They take shape of a horseshoe  Globe deformations and torsion leading to PVD and fluid collects subsequently in the subretinal space
  • 67.
    Necrotic Retinal Breaks Seen posterior to ora serrata  Direct contusive damage, retinal vascular damage and retinal capillary necrosis leads to weakened retina and irregularly shaped retinal breaks  Detachment tends to form within 24 hours
  • 68.
    Vitreous Base Avulsion Occurs commonly after blunt trauma  Associated with pars plana tears, retinal dialysis, retinal tears  Bucket handle appearance- stripe of translucent vitreous over the retina  May be asymptomatic, but should search for associated conditions
  • 69.
    Treatment  Wait andwatch  Prophylactic laser retinopexy/ trans-scleral cryopexy- peripheral retinal breaks  Aim of surgery- close all retinal breaks and relieve vitreoretinal traction  Surgical techniques- pneumatic retinopexy, scleral buckling and/or PPV  Giant retinal tears- PFC stabilization, lensectomy, , silicon oil tamponade  RD with pars plana tears/ retinal dialysis- scleral buckling with trans-scleral cryotherapy or PPV, air-fluid exchange, internal drainage of SRF and endolaser photocoagulation
  • 70.
    Traumatic Optic Neuropathy Intracanalicular part is most vulnerable  Mechanism of damage to optic nerve  Direct deformation of skull and optic canal  Shearing of ON microvasculature  Tearing of nerve axons  Contusion against optic canal  Presentation  Profound visual loss, loss of centralVA  Visual field defects  RAPD  Colour vision defects  Management  CT gold standard  Observation  High dose corticosteroids -IV methylprednisolone 30 mg/kg f/b 15 mg/kg 6 hourly  Optic canal decompression
  • 71.
    Orbital Trauma  Orbitalinjury can be contusive/ penetrating  Evaluation-  Periorbital oedema, lacerations, FB  Ptosis- edema, haemorrhage, neurogenic  Crepitus/bony discontinuity- orbital fractures  Enophthalmos-large orbital #  Exophthalmos- edema, haemorrhage, bony fragments, air  EOM- muscle entrapment, IR mostly involved  Check Sensations- infraorbital nerve distribution  Nasal passages- epistaxis, CSF rhinorrhea
  • 73.
     Blowout Fractures Expansion of orbital volume due to fracture of the thin orbital walls into adjacent paranasal sinuses  ‘Hydraulic theory’ and ‘buckling theory’  Axial and Coronal CT scan  Management  Systemic oral antibiotics, nasal decongestants, ice packs  Surgery indicated-  Entrapment of IR or perimuscular tissue with diplopia  Significant enophthalmos upto 7-10 days  High risk injuries for enophthalmos  Large floor/medial wall #  Combined medial wall and floor #
  • 74.
     Surgery-  MedialWall-Floor/ transcaruncular incision  Orbital floor  approached through transconjunctival/ sunciliary incision  Entrapped tissues are released  Orbital implant- nylon sheets, polyethylene, teflon, bone
  • 75.
    Open Globe Injuries Globe rupture- full thickness eyewall injury caused by blunt trauma  Laceration- full thickness eyewall wound caused by sharp object  Corneal laceration  Corneoscleral laceration  Scleral laceration
  • 76.
     Ophthalmic Examination 360 degreee sub-conjunctival haemorrhage  ‘Jelly Roll’ chemosis  Relative asymmetry in AC depth-  shallow in injuries ant to ciliary body  deep – post seg involvement  Transillumination defects in iris- path of projectile injuries  Violation of ant capsule, focal cataract  Seidel test  Rule outVH, IOFB, RD by dilated examination
  • 77.
    Management  Avoid manipulationof eye, put a protective shield over the injured eye  Timing of the surgery depends upon systemic condition of the patient  Repair can be performed under Peribulbar anaesthesia in adults and under GA in children  Start systemic antibiotics- IV aminoglycosides and 3rd generation cephalosporins
  • 78.
    Surgery  Examination ofeye under microscope and devise a surgical strategy  Goals  Close the globe with minimal manipulation  Reposit/ excise exposed intraocular contents  Explore the globe for unrecognized injuries  Decrease the risk of endophthalmitis and maximize chances of functional recovery by restoring ocular integrity
  • 79.
    Corneal Lacerations  Small,self-sealing clean corneal lacerations without iris incarceration- cyanoacrylate glue application  Large lacerations  Limbal paracentesis site created  Injection of viscoelastic substance in AC  Iris repositioned, if necrotic abscission required  Thorough wash with BSS  Sutures taken with 10-0 nylon, start with central suture  Wound divided in two halves at the pass of each suture  75% and 90% depth of suture pass optimal for healing  Depth equal on either side, adequate tension  Longer passes- less astigmatism  Adequate sutures in periphery, less near visual axis  Sutures rotated and buried once the wound is stabilized  Subconj inj antibiotic and steroid is given, eye patched and shield placed
  • 80.
    Corneoscleral Laceration  Largerwound with higher incidence of uveal prolapse or incarceration  Primarily stabilize the limbus by a 9-0 nylon suture  Repair in anterior to posterior direction
  • 81.
    Scleral Laceration  Identifythe posterior extent of the laceration  Dissect overlying conjunctiva andTenon’s capsule  Sutures taken with 8-0 or 9-0 nylon  Initially place one or two central sutures for easier repositioning of uveal tissue  Suture pass should be atleast 50% depth, full thickness passes avoided  Interrupted sutures preferred, ends are cut and rotated if possible
  • 82.
     Rectus musclelaceration- muscle is secured with double armed 6-0 vicryl, disinserted from globe, and resutured after wound closure to its original attachment  Posterior scleral lacerations  360 degree conjuctival peritomy  Isolate all recti on muscle hhoks and secure with loop of 2-0 braided polyester suture  Suturing performed, most post part may be leftto heal by secondary intention  Tissue loss- scleral or corneal patch graft  Conjunctiva closed with 6-0 vicryl
  • 83.
  • 84.
    Ruptured Globe Repair Exploratory surgery  360 degree conjunctival peritomy  Bipolar cautery for haemostasis  Wound closure performed as described earlier
  • 85.
    Post-operative Management  Thouroughclinical examination  Topical antibiotics, steroids, cycloplegics, tear substitutes  IOP lowering agents in case it is elevated  Eye shielded, avoid strenuous activities  Continue systemic antibiotics, shift to oral  Use of soft bandaged contact lenses  VR consultation in cases of  IOFB  Endophthalmitis  RD,VH  Posterior scleral rupture/ laceration  Choroidal detachment, dislocated lens  Frequent follow-ups  Suture removal after 4-6 weeks
  • 86.
    Complications and Outcomes Poor prognostic signs-  Initial visual acuity at presentation  Length and width of laceration  Lacerations of recti  Involvement of lens  VH, RD  Endophthalmitis, sympathetic ophthalmia  Irregular astigmatism- Rigid gas permeable contact lenses can be used
  • 87.
    Intraocular Foreign Bodies Penetrating ocular trauma with IOFB is a challenging situation for an ophthalmologist  Diagnosis requires thorough history, examination and proper imaging
  • 88.
     Ophthalmic examination Subconj haemorrhage, iris transillumination defects  Hyphema, focal lens opacity  Corneal/scleral laceration  Violation of ant or post lens capsule  VH, intra/ sub-retinal haemorrhage  Relative hypotony  Visible FB  Gonioscopy- FB in angle  Mainstay in imaging- USG and CT, preferably helical CT with 1mm cuts
  • 89.
    Management  Anterior chamberFB  Entry wound in cornea is closed as described earlier  Limbal paracentesis/ clear corneal incision made away from the wound  FB directly visualised, use of surgical gonioscopy lens (Koeppe’s lens)  Grasped with forceps and removed, may need bimanual manipulation  Metallic FB – use of intraocular magnet
  • 90.
     Intralenticular FB- can be managed by lens extraction by phacomulsification and forceps extracion of FB  Posterior segment FB  Immediate removal is advocated  Stabilization of the wound  Pars plana lens extraction  Stabilization and repair of retina  Forceps/ magnetic removal of FB  Scleral buckling, intravitreal injections
  • 91.
    Delayed Complications ofocular injury  Traumatic Iritis  Traumatic cataract  Delayed trauma-related glaucoma  Angle recession glaucoma  Vitreous haemorrhage- induced glaucoma  Lens- induced glaucoma  Retinal Detachment  Metallosis bulbi- siderosis bulbi, chalcosis  Sympathetic ophthalmia  Choroidal Neovascularization  Traumatic endophthalmitis
  • 92.
    Sympathetic Ophthalmia  Bilateralgranulomatous uveitis  MC following open globe injury (incidence 0.2 to 0.5%), may also occur after intraocular surgery  Pathophysiology-  Traumatic injury- uveal antigens are exposed- autoimmune response  Exciting/injured eye and sympathizing/ normal eye both become inflamed  A/w HLA-A 11 is shown  Onset- 2 weeks to 6 months after injury, mostly within 3 months
  • 94.
     Clinical Features Mild pain, photophobia, DOV  Mutton fat keratic precipitates  Granulomatous panuveitis with prominent vitritis  Choroidal lesions- multifocal, placoid, cream colored- Dalen Fuch’s nodules  Optic nerve hyperemia, swelling  FA- multiple hyperfluorescent sites leak in late phase  Management  Prevention- enucleation of severely injured eye  T/t-  High dose steroids with tapering  Cyclosporine, azathioprine, chlorambucil, methotrexate
  • 95.
    Traumatic Endophthalmitis  Incidence4-7%  Risk factors- IOFB, lens capsule violation, contamination, delayed primary repair  Presentation- pain, hypopyon, membranous vitreous opacities  Diagnosis- clinical  Organisms- Staph. Epidermidis, Bacillus cereus, Streptococcus  Treatment-  Vitreous aspiration for culture with intravitreal inj of antibiotics  PPV with intravitreal inj of antibiotics
  • 96.
    Non- Mechanical EyeInjuries  Chemical Injuries  Thermal Injuries  Ultrasonic Injuries  Electrical Injuries  Radiational Injuries
  • 97.
    Chemical Injuries  Trueocular emergencies, every second counts  Immediate irrigation is vital  Check pH in cul de sac if possible.  Type of chemical  Alkali- most severe damage- rapid penetration- saponification of cell membranes, denaturation of collagen  Acids- less damage- hydrogen ion precipitates proteins and prevents penetration
  • 98.
    Roper- Hall modificationof Hughes classification
  • 99.
     After thoroughirrigation, record visual acuity, IOP  Lids ,lashes- crystallized chemicals  Upper and lower fornix- swipe with cotton swab  Size of corneal epi defect, limbal ischemia in clock hours  AC reaction
  • 100.
     Management  Copiousirrigation underTA with liter bags of saline with monitoring of pH till pH neutralizes  Perform in a lying down position  Use retractors  Antibiotic eye ointments, cycloplegic, tear substitutes  Topical steroids with tapering  10 % ascorbate and 10% citrate e/d 2hrly  OralVit C 500mg  Oral Doxycycline 50-100mg BD- collagenase inhibitor  Control of raised IOP- topical beta blockers, alpha agonists,CA inhibitors  Monitor daily  SurgicalT/t- temporary tarsorrhaphy, corneal glue, patch graft
  • 101.
    Thermal Injuries  HyperthermalInjuries  Flame burns, contact burns  Clinical Presentations  Conj hyperemia, chemosis  Corneal superficial /deep burns- corneal opacification, sloughing  Healing- leucoma formation  Bullous keratitis, ectasia, staphyloma, symblepharon  Scleral involvement- uveal prolapse, uveitis, panophthalmitis
  • 102.
     Treatment  Cleanwith saline  Antibiotic cream  Full thickness burns of lid- grafting  Topical – atropine, antibiotics, lubricating e/d, steroids  Glass rod passed in fornices  Conj transposition flap, amniotic membrane graft, limbal cell transplant  PK or LK for leucomatous corneal opacity later stage
  • 103.
     Hypothermal Injuries Surgical Hypothermia-Cardiovascular/ neurosurgery  Accidental hypothermia  Cryosurgery  Clinical lesions  Conj congestion, edema  Muscle, tendons- edema and haemorrhage  Ciliary body- reduced aqueous formation  Adhesive chorioretinal traction, vitreous iceballs
  • 104.
    Electrical Injuries  Pointof entry and exit  Clinical Features-  Lid burns- entry wound  Corneal interstitial opacities  Iritis, miosis, spasm of accomodation  Electric cataract  Retinal edema, papilloedema, RD , chorioretinitis  Optic neuritis
  • 105.
    Radiational Injuries  Ionizingradiations- X rays, beta rays  Loss of lashes, entropion, ectropion  Conj scarring  Cataract  UV radiations  Damage to corneal epithelium  Cataract formation  Visible radiation  Thermal injuries  Sun gazing l/t damage to macula  Infrared radiation- Glassblower’s cataract  Welding arc injuries
  • 106.
    Prevention  Patient education Use of protective eyewear at workplaces and in sports activities  Use of helmet while riding two wheelers  Parent education to avoid eye injuries with household items in children  Safety norms should be introduced in workplaces regarding protection of eyes
  • 107.
    Take Home Message… Immediate treatment is directed at preventing further injury or vision loss  Never think of the eye in isolation, always compare both eyes  Always record visual acuity as it has important medicolegal implications  A visual acuity of 6/6 does not necessarily exclude a serious eye injury  Beware of the unilateral red eye as it is rarely ‘just’ conjunctivitis  Documentation  Use of protective eyewear
  • 108.
    References  Indian JOphthalmol. 2013 Oct; 61(10): 539–540 PMCID: PMC3853447 Ocular trauma, an evolving sub specialty Sundaram Natarajan  Ngrel AD, Thylefors B. The global impact of eye injuries [J] Ophthalmic Epidemiol. 1998;5:143–69. PubMed  Ocular trauma by James T. Banta  Clinical Diagnosis and management of ocular trauma by Garg, Moreno, Shukla et al