Trauma




Eyelid Trauma


Periocular haematoma


A ‘black eye’, consisting of a haematoma (focal collection of blood) and/or periocular ecchymosis (diffuse bruising) and oedema ( Fig. 21.1A ) is the most common blunt injury to the eyelid or forehead and is generally innocuous. It is, however, critical to exclude the following more serious conditions:




  • Trauma to the globe or orbit. It is easier to examine the globe before the lids become oedematous. Once swelling is established, gentle sustained pressure to open the lids will often displace tissue fluid sufficiently to allow visualization of the anterior segment; it is critical not to allow any force on the globe itself until its integrity has been confirmed. Imaging such as computed tomography (CT) or magnetic resonance imaging (MRI) if rapidly available, or bedside ultrasonography (strictly avoiding pressure on the globe), should be considered if there is suspicion of an underlying injury to the eyeball and adequate clinical visualization is not possible.



  • Orbital roof fracture , especially if the black eye is associated with a subconjunctival haemorrhage without a visible posterior limit ( Fig. 21.1B ), which sometimes indicates anterior extension from a posterior bleeding point.



  • Basal skull fracture , which may give rise to characteristic bilateral ring haematomas (‘panda eyes’ – Fig. 21.1C ).




Fig. 21.1


(A) Upper lid haematoma, periocular ecchymosis and oedema; (B) subconjunctival haemorrhage with no visible posterior limit; (C) ‘panda eyes’






Laceration


The presence of a lid laceration, however insignificant, mandates careful exploration of the wound and examination of the globe and adnexal structures. Any lid defect should be repaired by direct closure whenever possible, even under tension, since this affords the best functional and cosmetic result ( Fig. 21.2 ).




  • Superficial lacerations parallel to the lid margin without gaping can be sutured with 6-0 black silk or nylon; the sutures are removed after 5–6 days.



  • Lid margin lacerations invariably gape without careful closure and to prevent notching must be sutured with optimal alignment ( Fig. 21.3 ):



    • a.

      A 5-0 silk vertical mattress suture is inserted in line with the meibomian gland orifices, about 2 mm from the wound edges and 2 mm deep, and left untied.


    • b.

      Tarsal plate edges are apposed with partial-thickness lamellar 5-0 absorbable (e.g. polyglactin) sutures, which are tied anteriorly.


    • c.

      The lid margin silk suture is then tied so that the cut edges slightly pucker the wound; the ends are left fairly long, e.g. 2 cm.


    • d.

      The overlying skin is closed with interrupted 6-0 or 7-0 nylon or absorbable sutures, securing the ends of the silk suture to direct these and its knot away from the cornea.




    Fig. 21.3


    Repair of full-thickness lid laceration. (A) Initial approximation of the tarsal plate with an absorbable suture and lid margin with a silk suture; (B) completed repair – note that with a laceration near the canaliculus its involvement must be excluded

    (Courtesy of J Nerad, K Carter and M Alford, from ‘Oculoplastic and Reconstructive Surgery’, in Rapid Diagnosis in Ophthalmology , Mosby 2008)





  • Lacerations with mild tissue loss just sufficient to prevent direct primary closure can usually be managed by performing a lateral cantholysis in order to increase lateral mobility.



  • Lacerations with extensive tissue loss may require major reconstructive procedures similar to those used following resection of malignant tumours (see Ch. 1 ).



  • Canalicular lacerations should be repaired within 24 hours. The laceration is bridged by silicone tubing (Crawford tube), which is threaded down the lacrimal system and tied in the nose, following which the laceration is sutured. Alternatively, repair of a single canaliculus can be performed using a monocanalicular stent (e.g. Mini Monoka – Fig. 21.4 ) and, if necessary, suturing its footplate to the lid using 8-0 material. The tubing is left in situ for 3–6 months.




    Fig. 21.4


    Monocanalicular silicone stent

    (Courtesy of S Chen)



  • Tetanus status. It is critical to ensure that the patient’s tetanus immunization status is satisfactory after any injury. Without any prior immunization, 250 units of human tetanus immunoglobulin are given intramuscularly (IM); if previously immunized but a booster has not been administered within the last 10 years, IM or subcutaneous tetanus toxoid is given.




Fig. 21.2


Upper lid laceration. (A) Prolapsed fat gives an indication that the wound is of substantial depth; (B) failure of upgaze in the eye suggests damage to the levator muscle; (C) skin sutures following levator repair – this necessitated extension of the laceration

(Courtesy of S Chen)








Orbital Trauma


Orbital floor fracture


Introduction


A blow-out fracture of the orbital floor is typically caused by a sudden increase in the orbital pressure from an impacting object that is greater in diameter than the orbital aperture (about 5 cm), such as a fist or tennis ball, so that the eyeball itself is displaced and transmits rather than absorbs the impact ( Fig. 21.5 ). Since the bones of the lateral wall and the roof are usually able to withstand such trauma, the fracture most frequently involves the floor of the orbit along the thin bone covering the infraorbital canal. Occasionally, the medial orbital wall may also be fractured; fractures of the orbital rim and adjacent facial bones require appropriately tailored management. Clinical features vary with the severity of trauma and the interval between injury and examination. Care should be taken to ensure that a full evaluation for head and systemic injury has been performed, and any necessary interspecialty referrals initiated.




Fig. 21.5


Mechanism of an orbital floor blow-out fracture


Diagnosis





  • Visual function , especially acuity, should be recorded and monitored as necessary, particularly in the acute situation.



  • Periocular signs include variable ecchymosis, oedema ( Fig. 21.6A ) and occasionally subcutaneous emphysema (a crackling sensation on palpation due to air in the subcutaneous tissues).




    Fig. 21.6


    Right orbital floor blow-out fracture. (A) Marked periocular ecchymosis, oedema and subconjunctival haemorrhage; (B) restricted elevation; (C) mild right enophthalmos

    (Courtesy of S Chen – fig. A)







  • Infraorbital nerve anaesthesia involving the lower lid, cheek, side of nose, upper lip, upper teeth and gums is very common as the fracture frequently involves the infraorbital canal.



  • Diplopia may be caused by one of the following mechanisms:




    • Haemorrhage and oedema in the orbit may causing the septa connecting the inferior rectus and inferior oblique muscles to the periorbita to become taut, thus restricting movement of the globe. Ocular motility usually improves as the haemorrhage and oedema resolve.



    • Mechanical entrapment within the fracture of the inferior rectus or inferior oblique muscle, or adjacent connective tissue and fat. Diplopia typically occurs in both upgaze ( Fig. 21.6B ) and downgaze. Forced duction and the differential intraocular pressure (IOP) test (increasing IOP as a restricted muscle presses on the globe) are positive. Diplopia may subsequently improve if it is mainly due to entrapment of oedematous connective tissue and fat, but usually persists if there is significant involvement of the muscles themselves.



    • Direct injury to an extraocular muscle, associated with a negative forced duction test. The muscle fibres usually regenerate and normal function often returns within about 2 months.




  • Enophthalmos ( Fig. 21.6C ) may be present if the fracture is severe, although it tends to manifest only after a few days as initial oedema resolves. In the absence of surgical intervention, enophthalmos may continue to increase for about 6 months as post-traumatic orbital tissue degeneration and fibrosis develop.



  • Ocular damage (e.g. hyphaema, angle recession, retinal dialysis) should be excluded by careful examination of the globe, although this is relatively uncommon in association with a blowout fracture.



  • Hess chart testing ( Fig. 21.7 ) to map eye movements is useful in assessment and monitoring.




    Fig. 21.7


    Hess chart of a left orbital floor blow-out fracture shows restriction of left upgaze (superior rectus and inferior oblique) and restriction on downgaze (inferior rectus). There is also secondary overaction of the right eye



  • CT with coronal sections ( Fig. 21.8 ) aids in evaluation of the extent of a fracture and determination of the nature of maxillary antral soft-tissue densities, which may represent prolapsed orbital fat, extraocular muscles, haematoma or unrelated antral polyps.




    Fig. 21.8


    CT of right orbital floor blow-out fracture – coronal view shows a defect in the orbital floor (arrow) and the ‘tear drop’ sign due to soft tissue prolapse into the maxillary antrum

    (Courtesy of A Pearson)



Treatment





  • Initial treatment generally consists of observation, with the prescription of oral antibiotics; ice packs and nasal decongestants may be helpful. The patient should be instructed not to blow his or her nose, because of the possibility of forcing infected sinus contents into the orbit. Systemic steroids are occasionally required for severe orbital oedema, particularly if this is compromising the optic nerve.



  • Subsequent treatment is aimed at the prevention of permanent vertical diplopia and/or cosmetically unacceptable enophthalmos.




    • Small cracks unassociated with herniation do not require treatment as the risk of permanent complications is small.



    • Fractures involving up to one-half of the orbital floor, with little or no herniation, no significant enophthalmos and improving diplopia, also do not require treatment.



    • Fractures involving more than one-half of the orbital floor will usually develop significant enophthalmos if left untreated.



    • Fractures with entrapment of orbital contents, enophthalmos of greater than 2 mm, and/or persistent and significant diplopia in the primary position should be repaired within 2 weeks. If surgery is delayed, the results are less satisfactory due to secondary fibrotic changes.




  • ‘White-eyed’ fracture is a subgroup for which urgent repair is required to avoid permanent neuromuscular damage. The scenario is generally seen in patients less than 18 years of age, typically with little visible external soft tissue injury, and usually affects the orbital floor. It involves the acute incarceration of herniated tissue in a trap-door effect occurring due to the greater elasticity of bone in younger people. Patients may experience acute nausea, vomiting, and headache; persistent activation of the oculocardiac reflex can occur. CT features may be subtle.



  • Early marked enophthalmos may also be an indication for urgent repair.



  • Surgical repair is performed via a transconjunctival or subciliary incision or via the maxillary sinus, with elevation of the periosteum from the orbital floor, freeing of trapped orbital contents and repair of the bony defect with a synthetic implant.



Roof fracture


Introduction


Roof fractures are rarely encountered by ophthalmologists. Isolated fractures, caused by falling on a sharp object ( Fig. 21.9 ) or sometimes a relatively minor blow to the brow or forehead, are most common in children and often do not require treatment. Fractures due to major trauma, with associated displacement of the orbital rim or significant disturbance of other craniofacial bones, typically affect adults.




Fig. 21.9


Preoperative image of a patient with an orbital roof fracture caused by a ball-point pen

(Courtesy of R Bates)


Diagnosis


A haematoma of the upper eyelid is typical, together with periocular ecchymosis; these often develop over the course of a few hours and may progressively spread to the side opposite the fracture. Other features of orbital wall fracture as discussed above may be present. Large fractures may be associated with pulsation of the globe due to transmission of cerebrospinal fluid (CSF) pressure, best detected with applanation tonometry.


Treatment


Small fractures may not require treatment but it is important to exclude a CSF leak, which carries a risk of meningitis. Sizeable bony defects with downward displacement of fragments usually warrant reconstructive surgery. General management is similar to that of an orbital floor fracture (see above).


Blow-out medial wall fracture


Medial wall orbital fractures are usually associated with floor fractures; isolated fractures are relatively uncommon. Signs include periorbital ecchymosis and frequently subcutaneous emphysema, which typically develops on blowing the nose. Defective ocular motility involving abduction and adduction is present if the medial rectus muscle is entrapped. CT will demonstrate the fracture; treatment involves release of incarcerated tissue and repair of the bony defect.


Lateral wall fracture


Acute lateral wall fractures (see Fig. 21.11F ) are rarely encountered by ophthalmologists. Because the lateral wall of the orbit is more solid than the other walls, a fracture is usually associated with extensive facial damage.


Orbital haemorrhage


Introduction


Orbital (retrobulbar) haemorrhage is important chiefly due to the associated risk of acute orbital compartment syndrome with compressive optic neuropathy, and can lead to irreversible blindness of the affected eye in severe cases. It can occur without or in association with an orbital bony injury. Iatrogenic orbital haemorrhage is not uncommon, typically resulting from a peri- or retrobulbar local anaesthetic block performed to facilitate intra­ocular surgery. Rare causes include bleeding from vascular anomalies and occasionally spontaneous haemorrhage due to poor clotting.


Diagnosis


Proptosis, eyelid oedema and ecchymosis, haemorrhagic chemosis, ocular motility dysfunction, decreased visual acuity, elevated intraocular pressure, optic disc swelling and a relative afferent pupillary defect are among the possible signs.


Treatment


Treatment should be immediate when progressive visual deterioration is evident. Canthotomy alone is rarely adequate.




  • Canthotomy. After clamping the incision site for 60 seconds, scissors are used to make a 1–2 cm horizontal full-thickness incision under local anaesthesia (e.g. 1–2 ml lidocaine 1–2% with adrenaline) at the angle of the lateral canthus ( Fig. 21.10A ).




    Fig. 21.10


    Surgical treatment of acute retrobulbar haemorrhage. (A) Lateral canthotomy; (B) disinsertion of inferior crus of the lateral canthal tendon

    (Courtesy of K Goodall, A Brahma, A Bates, B Leatherbarrow, from International Journal of the Care of the Injured 1999;30:485-90)





  • Cantholysis. Following canthotomy, the lower lid is retracted downwards and the inferior crus of the lateral canthal tendon transected ( Fig. 21.10B ) using blunt-tipped scissors, directed inferiorly and inserted adjacent and parallel to the lateral orbital rim between conjunctiva and skin, and angled away from the eyeball. Blood is gently encouraged to drain. If necessary the superior limb of the tendon can also be transected, but this carries a substantial risk of damage to adnexal structures.





Trauma to the Globe


Introduction


Terminology





  • Closed injury is commonly due to blunt trauma. The corneoscleral wall of the globe is intact.



  • Open injury involves a full-thickness wound of the corneoscleral envelope.



  • Contusion is a closed injury resulting from blunt trauma. Damage may occur at or distant to the site of impact.



  • Rupture is a full-thickness wound caused by blunt trauma. The globe gives way at its weakest point, which may not be at the site of impact.



  • Laceration is a full-thickness defect in the eye wall produced by a tearing injury, usually as the result of a direct impact.



  • Lamellar laceration is a partial-thickness laceration.



  • Incised injury is caused by a sharp object such as glass or a knife.



  • Penetrating injury refers to a single full-thickness wound, usually caused by a sharp object, without an exit wound. A penetrating injury may be associated with intraocular retention of a foreign body.



  • Perforation consists of two full-thickness wounds, one entry and one exit, usually caused by a missile.



Investigations





  • Plain radiographs may be taken when the presence of a foreign body is suspected ( Fig. 21.11A ).




    Fig. 21.11


    Imaging of ocular trauma. (A) Plain radiograph showing a lead air gun pellet; (B) foreign body demonstrated by ultrasonography; (C) CT axial and (D) coronal views localizing a left intraocular foreign body; (E) 3D CT reconstruction of a facial shotgun injury; (F) CT axial view demonstrating a left lateral orbital wall fracture

    (Courtesy of S Chen – figs C–E; A Pearson – fig. F)













  • Ultrasonography may be useful in the detection of intraocular foreign bodies ( Fig. 21.11B ), globe rupture, suprachoroidal haemorrhage and retinal detachment; it should be performed as gently as possible if there is the risk of an open globe injury, strictly avoiding any pressure on the globe. It is also helpful in planning surgical repair, for example guiding placement of infusion ports during vitrectomy and assessing whether drainage of suprachoroidal haemorrhage is required.



  • CT is superior to plain radiography in the detection and localization of intraocular foreign bodies ( Figs 21.11C and D ). It is also of value in determining the integrity of intracranial, facial and intraocular structures ( Figs 21.11E and F ).



  • MRI is more accurate than CT in the detection and assessment of injuries of the globe itself, such as an occult posterior rupture, though not for bony injury. However, MRI should not be performed if a ferrous metallic foreign body is suspected.



  • Electrodiagnostic tests may be useful in assessing the integrity of the optic nerve and retina, particularly if some time has passed since the original injury and there is the suspicion of a retained intraocular foreign body (IOFB).



Blunt trauma


The most common causes of blunt trauma are squash balls, elastic luggage straps and champagne corks. Severe blunt trauma to the globe results in anteroposterior compression with simultaneous expansion in the equatorial plane ( Fig. 21.12 ) associated with a transient but severe increase in IOP. Although the impact is primarily absorbed by the lens–iris diaphragm and the vitreous base, damage can also occur at a distant site such as the posterior pole. The extent of ocular damage depends on the severity of trauma and tends largely to be concentrated to either the anterior or posterior segment. Apart from obvious ocular damage, blunt trauma commonly results in more obscure long-term effects; the prognosis is therefore necessarily guarded.




Fig. 21.12


Pathogenesis of ocular damage by blunt trauma


Cornea



Aug 25, 2019 | Posted by in OPHTHALMOLOGY | Comments Off on Trauma

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