TRAUMA NOTES

                                          TRAUMA

INERT FOREIGN BODIES-

• Carbon
• Coal
• Lead
• Plaster
• Platinum
• Porcelain
• plastic
• Rubber
• Silver
• Stone

                   CHEMICAL INJURIES-cases

CAUSES-

• Industrial / agricultural
• Domestic accidents
• Assaults
• Chem warfare.

• Alkali burns-2MC
• Acid burns

ALKALIS-

• Ammonia
• Sodium hydroxide
• Lime
• Caustic soda
• Caustic potash
• Ammonium hydroxide is the most dangerous & lime is the least

    ACIDS-

• Sulphuric acid (used in battery)-dangerous as it penetrates deep like alkali
• Sulphurous acid
• Hydrofluoric acid
• Hydrochloric acid
• Acetic acid
• Chromic acid
• Nitric acid.

PATHOGENESIS-

ACIDS→ coagulation of proteins→ insoluble acid albuminate

→protective barrier to penetration→damage is restricted

                                                       -Lesions –sharply demarcated

                                                       -Non-progressive

ALKALIS→

• OH Grp of alkalis→Saponification of fatty acids of the cell memb→ cell death→ disruption of epith barrier→ deeper penetration into stroma
• Cations of alkali + COOH [collagen & stromal glycosaminoglycans]→ swelling,thickening & shortening of coll fibrils→ rise in IOP,increase succeptibility of coll to enzymatic degradation
• Denaturation of mucoid
• Thus alkalis are serious& hav a poor prognosis

PATHOPHYSIOLOGY-

• occlusion of limbal vasculature→ necrosis of cor & conj epith→loss of limbal stem cells→ conjunctivalization +   

                                                        cor vascularisation

 * loss of limbal stem cells→sterile cor ulceration→perforation

• Glycosaminoglycans→ breakdown & pptn→ stromal opacification
• AC penetration → damage to lens & iris
• Ciliary epith damage→ decrease sec of ascorbate which is concerned with collagen prod & cor repair
• Ciliary epith damage → reduces aq sec→ hypotony

GRADING-Hughes & Roper hall class

• I –No limbal ischaemia
• II < 180 deg limbal ischaemia

               -Clear cor

              -Epith defect

   *   III > 180deg limbal ischaemia

              -Hazy cor

              -epith defect

    *  IV > 270 deg limbal ischaemia

            -Hazy cor

            -Epith defect

C/F=1st week-Acute phase

• Conj congestn &chemosis
• Perilimbal ischaemia
• Cor epith def & stromal clouding
• Rise in IOP

2-3 weeks-early reparative phase

- Cor & conjepith begin to regenerate

- Cor opacity + vascularization

- Iridocyclitis

3weeks-mo –Late reparative phase

-Irreg scarring of cor

-Cor ulcer & descemetocele→ perforation

- Dry eye d/t scarring of lacrimal gld ducts & goblet cells

-Post synechiae & cyclitic memb

- Cataract

-CB atrophy→ hypotony→ phthisis bulbi

-Entropion,trichiasis & symblepharon

T/T-

1. First aid- Liberal wash with weak acetic acid soln, water / NS for 30 min or till pH becomes neutral [ 7].min 1 lit ( avg 8-10 lit)
2. Thorough SLE-lime particles picked up with forceps/cotton bud & search the fornices by double eversion
3. Analgesics
4. Cycloplegic- Atropine 1 % e/o tds
5. Sys & topical antibiotic-T . Tetracycline/ Doxy 100mg BD→ Inhibit collagenase & neutrophil→ reduce ulcern
6. T acetazolamide & topical b blocker e/d
7. Daily sweeping of a glass rod around the fornices-For symblepharon→ scleral shell or ring to maintain fornices
8. topical pred acetate 1% or dexamethasone 0.1% 2-3 hrly –for significant inflamn of AC or cor
9. Topical Ascorbic acid ( renal toxicity)→ fibroblast → lay down collagen-Topical sodium ascorbate 10% 2 hrly & oral- 2gm qid
10. Acetic acid & citric acid 10 % e/d
11. acetyl cysteine ( 10-20 % e/d) for cor melting

10.BSCL

11.Tear substitutes

12.Tiss adhesives if cor melting progresses

13.Correction of lid deformity

14.Amniotic membrane transplant-in acute phase gives better results

   15.Limbal stem cell graft

    16.Therapeutic  KP

   17. Keratoprosthesis

    SYMPATHETIC OPHTHALMITIS

DEF-

This is a condition in which serious inflamn attacks the sound eye after injury to the other eye.

  Surgical trauma/ Penetrating inj→ BL granulomatous panuveitis

IMMUNOLOGICAL CONSIDERATIONS-

-Cell mediated autoimmune response to retinal,RPE or choroidal antigen [eg retinal “ S” antigen tyrosinase related protein]

-A penetrating wound with uveal prolapse permits tolerated ocular antigen to reach dendritic cells,or the so-called professional antigen presenting cells,outside of the eye,when there is an inflammatory stimulus.Bcos the antigen presenting cells appear to be functionally suppressed in situ,these antigens would produce an inactivation signal.

AETIO-

1. Almost always results from a penetrating wound with iris,Cb or lens capsule incarcerated within the scar.
2. Elective surg for cat / glauc .
3. After proton beam irradiation
4. Nd:YAG cyclophotocoagulation
5. Cyclocryotherapy

EPID-

• Childn are particularly susceptible
• Begins 4-8 wks after inj to the first eye [ exciting eye ]
• Sound eye→ Sympathetizing eye
• Autoimmune T- cell mediated dis.Uveal pigment acts as an allergen

PATHOLOGY-

• Nodular aggreg of lymphocytes & plasma cells scattered thru out the uveal tr
• Pigment epith of iris & CB proliferate to form nodular aggreg→ DALEN FUCH’S NODULES
• Retina becomes infiltrated with lymphocytes & plasma cells in the neighbourhood of BVs

C/F-

• Exciting eye- Plastic iridocyclitis does not subside even in 3-4 wks.-Ciliary inj

              -Lacrimation

              -Tenderness

*  Sympathizing eye-

- Pain

-photophobia

-Diff in near vision [ D/t loss of accommodation]-Earliest symptom

SIGNS-

• Retrolental flare  [Earliest sign]
• Mutton-fat KPs
• Iris nodules
• Post synechiae
• Sec glaucoma
• Fundus-Dalen Fuch’s nodules[Small,deep,Yellow-white spots scattered]
• Perivasculitis
• Retinal edema
• choriocapillaries typically spared
• Exud RD
• Papillitis

COMPLICATIONS-

• Cataract
• Sec glaucoma
• Phthisis bulbi
• Blindness

T/T-

1.  Steroids-Topical-Dexamethasone 0.1 % e/d

                 -Sub-tenon triamcinolone acet / methyl pred 40mg/ml

                 -IV methyl prednisolone 1gm for 3 days→ oral prednisone 1mg/kg/day for 11 days

2. Immunosuppressants-Cyclosporin –A 2-5 mg/kg/day-very effective

3Cycloplegics

4. Closure of penetrating wound

5. If injured eye is unsalvageable→ Enucleation within 2 wks foll inj

Diff from VKH syn-

1. H/o trauma.
2. Choriocapillaries not inv

       BLOW OUT # - ORBIT

Blow out # occurs when the orbital walls are pressed indirectly.

Mainly inv –Orbital floor

                 -Medial wall

CLASS-

1] Depending on the #d bones-

*  Pure blow out #  - orbital rim not inv

*  Impure blow out #  - orbital floor + Middle –third of facial skeleton

2] Depending on the extent of #-

1)  Egg-shell BO #-

    Hammock like sagging of the floor into the maxillary antrum

2)  Trap- door BO # -

    Trap door piece of bone hangs on a periosteal hinge into the max sinus

3)  Linear BO # -

    Pinches the orbital contents

4) BO # with a large opening into max sinus-

   Herniation of orbital contents into the max antrum

MECHANISM OF BO #-

1] Trauma by a large & round object( tennis ball,cricket ball,human fist)→ Blunt inj→ Backward displacement of eyeball→ increase in intraorbital press →# weakest point of the orb wall-Floor & Medial wall [in the region of lamina papyracea ]→ herniation of soft tiss into max antrum→ IR / IO may be caught → impaired OM

2] Blow on the orbital rim→ transmitted as a buckling force along the orb floor→ Linear / Frank #--> Orbital fascia gets trapped in the # or ruptured tiss herniated thru the defect.

C/F-

• Periorbital edema
• Ecchymosis
• Emphysema of lid-Mc with # med wall & made worse by blowing nose
• Paraesthesia –area of infraorbital N-LL,Cheek,side of nose,upper lip &upper teeth
• .Epistaxis-d/t bleeding from max sinus into nose
• Proptosis-d/t emphysema,edema & h’age→ 10 days later→
• Enophthalmos- d/t –

1. Escape of orbital fat into max sinus
2. Backward traction on globe by entrapped IR
3. Displacement of fragments→ enlargement of cavity

• Diplopia-typically in up & down gaze-Double diplopia

Causes-

1.Entrapment of IO/IR

2.Injury to motor Ns

3.Direct inj to ms by bone fragment

4. Ms disruption from its attachment→ H’age into the ms

Ms restriction can be confirmed by-

1. Forced duction test
2. Differential IOP test [see orbit-proptosis evaln]

FORCED DUCTION TEST-

• Topical anaesthesia
• Grasp the IR 7 mm from the limbus
• Rotate the globe upwards
• Positive- Globe cannot be rotated up d/t incarceration of IR in the lips of BO #

Examine for IO damage-

• Hyphaema
• Traumatic iridodialysis
• Contusion cataract
• Lens subluxation
• Angle recession
• VH
• Retinal dialysis
• Giant retinal tear
• Commotio retinae
• Pre-ret h’age

INV-

1. PLAIN X-RAY-

• Most useful view- Water’s view

Others- Caldwell

          -Fronto-occipital

           -Oblique

            -AP

* Findings-

-Fragmentation & irregularity of orb floor

-Depression of bony fragments

-“Hanging drop” opacity of the superior maxillary antrum from orb contents herniating thru the floor.

2.CT SCAN-

*  For detailed visualization of soft tiss

*  Coronal sec- Extent of #

                      -Nature of soft tiss density

3. Hess test-monitoring progression of diplopia

4. Binocular field of vision

T/T-

Optimum time-

Within 10-14 days of injury.By this time ,local edema & periorbital edema & haematoma settle & fibrosis reduces→ allows adequate exam

Alternative view-

It is recommended that all pure BO # be foll for 4-6 mo without surg. Later Putterman modified this recommending that all such #s  be foll without surg until diplopia & enophthalmos hav stabilized.

Aim of t/t—

To prevent permanent vertical diplopia & enophthalmos.

IND OF SURGERY-

1. Non-resolving diplopia
2. # with large herniation of tiss into the antrum
3. Incarceration of tiss→ globe retraction
4. Increased iop on upgaze
5. Enophthalmos > 2mm

    SURGICAL APPROACH-

1. Thru the eyelid- Preferred as it permits easy disengagement of entrapped orb tiss.
2. Thru the canine fossa & max sinus→ For removal of bone fragments in the max sinus.

INCISION SITE FOR EYELID APPROACH-

1. Below the lash margin ( 3mm)-MC-Leaves an inconspiquous scar & allows easy exposure.
2. Lower lid line
3. Inferior orb rim
4. Conj cul de sac.

    EXPOSURE OF ORBITAL FLOOR-

    Incision made thru skin & orbicularis → Tarsus reached→ Septum orbitale becomes visible→ Dissection continued till orb rim reached → Periosteum incised below the orbital rim & elevated → Orbital floor exposed→ avoid inj to infraorbital N → Entrapped orb contents released

RESTORATION OF CONTINUITY OF ORBITAL FLOOR-

IMPLANTS-

• Bone graft
• Alloplastic implant
• Teflon sheets
• Supramid

Teflon –Tends to slide forwards & protrude under the skin of eyelid→ Therefore implant shud be anchored to the orb rim with a stable steel wire or make a tongue of the implant & introduce it under the ant edge of bony defect.