Some common periorbital problems:
• Double vision
• Pain (see also Chapter 10)
Common problems and their causes
(See also Chapter 10.)
Useful questions and what to look for
Examination of the cheek and orbit is not complete without an examination of the eye itself. This latter part of the examination is discussed in detail in Chapter 10 on the eye but is noted briefly here.
The ‘cheek bone’ is formed predominantly by the zygomatic bone. This has a superior process, which fuses with the frontal bone at the frontozygomatic suture just at the lateral aspect of the eyebrow. This is a key site in examination; tenderness and step deformity suggest a fracture of the cheek. Medially, the zygoma joins with the maxilla approximately two-thirds of the way along the infraorbital rim. This provides support for the lower eyelid. Lower down anteriorly, the cheek bone fuses with the anterior wall of the maxilla, passing medially to form the piriform (nasal) aperture. The lower lateral aspect of this bony complex (often referred to as the ‘buttresses’) can be palpated from within the mouth, just above the roots of the upper premolar and molar teeth. Tenderness and step deformity of this buttress suggest a fracture of the cheek. Bruising may also be visible.
The body of the zygoma forms the prominence of the cheek. Together with the supraorbital ridge it provides a degree of protection to the globe. The bones in this region also provide support to the soft tissues, notably the lower eyelid and the medial and lateral canthal tendons. Displacement of the bones results in obvious asymmetry and a vertical drop in the position of the lateral canthus, sometimes termed an ‘antimongoloid slant’. There may also be hypoglobus. The zygomatic arch is a key ‘strut’ in maintaining the forward projection of the cheek. Its importance can be overlooked when assessing facial X-rays.
This is a pyramidal-shaped structure enclosed by four bony walls—the roof, floor, medial, and lateral walls. These converge at the orbital apex. The globe is a round ball approximately 24 mm in diameter which occupies only about a quarter of the orbital volume. The remainder is made up of the lacrimal apparatus, muscles, fat, blood vessels, and nerves. The cornea of the globe is bathed in tears which originate from the lacrimal gland (upper lateral aspect of the orbit) and pass across the cornea in a medial direction towards the punctae. From there they pass through the canaliculi and lacrimal sac, which sits in a bony recess, the lacrimal fossa, before passing into the nose.
The walls of the orbit are of varying thickness and strengths. The medial orbital wall is particularly thin and perforated by numerous valveless blood vessels and nerves through a number of defects (Zuckerkandl dehiscences). This allows for easy communication of infectious material between the ethmoidal air cells and orbital soft tissues. The vessels here can bleed profusely into the orbit following trauma, which can result in a retrobulbar haematoma. Sensation to the cheek and lateral nose comes from the infraorbital nerve which passes along the orbital floor. Sensation to the forehead is from the supraorbital and supratrochlear nerves, both arising from the ophthalmic division of the trigeminal nerve. All these nerves are at risk of injury following either trauma to the orbit or from other intra-orbital pathology.
The upper part of the orbit is also part of the frontal bone. Significant force is required to fracture this bone. Injuries to this area may therefore be associated with dural tears, CSF leakage, and brain or cervical injury. The lateral wall of the orbit is composed of the zygoma and greater wing of the sphenoid (part of the middle cranial fossa). The most common injury in this region is fracture of the zygomatic bone.
Where the infra-orbital nerve passes along the floor of the orbit, the bone is especially weak. Isolated fractures of the orbital floor, or those associated with fractures of the zygoma, usually pass along this canal. Numbness of the cheek and upper lip is therefore an important sign that could indicate an underlying fracture. Occasionally the orbital contents herniate out following fracture of the orbital floor or medial wall. This is mostly periorbital fat but occasionally the extraocular muscles herniate. Entrapment prevents the coordinated action of the ocular muscles and may result in restricted eye movements and double vision (diplopia).
There are six striated muscles responsible for moving the eye: the four recti muscles (medial, lateral, superior, and inferior) and the superior and inferior oblique muscles. The nerves supplying these are the oculomotor, trochlear, and abducens nerves—‘SO4(LR6)3’ indicates the individual muscle innervations. The recti muscles have a common point of origin along the tendinous ring at the orbital apex. From there they pass forwards forming a muscular cone before inserting into the sclera. This cone can act as a closed compartment and contain blood following surgery or trauma (RBH).
The optic nerve runs from the back of the globe to the orbital apex and enters the cranial cavity via the optic foramen. Running in the opposite direction within this foramen is the ophthalmic artery which is a branch of internal carotid artery. The remaining blood vessels and nerves to the orbital contents gain access to the orbit via the superior orbital fissure.
Anteriorly the orbit is enclosed and protected by the eyelids. The upper eyelid is the most mobile and is elevated by the combined actions of a smooth muscle and a striated muscle (Müller’s muscle and levator palpebrae superioris respectively). The orbital septum is a layer of fascia extending vertically from the peripheral periosteum of the orbital rim into the levator aponeurosis in the upper eyelid and the inferior border of the tarsal plate in the lower eyelid. This is important as infection that passes deep to the septum can enter the orbit, resulting in orbital cellulitis. Eyelid and periorbital swellings therefore require prompt diagnosis and management.
(See also Chapter 10.) The face should be inspected from the front and side of the patient. It should also be viewed from above, looking down over the brow. With all orbital-related conditions, early assessment of the eye is essential as management initially takes priority. If the eyelids are closed due to painful swelling, gently pressing on the eyelids (not the globe) for a few minutes can often reduce swelling sufficiently to assess the eye. However, be careful if the swelling is thought to be due to cellulitis or an abscess. If necessary, a Desmarres retractor, lid speculum, or even a bent sterile paper clip can be used to gently retract the eyelids, while avoiding pressure on the globe. If necessary, apply topical anaesthetic (either tetracaine or proparacaine drops) to decrease discomfort. When there is significant swelling, assessment of the eye can be limited. As a minimum, make sure you assess visual acuity, pupils, extraocular motility, and visual fields. Never allow a patient with orbital pathology to go home if you have been unable to assess the eye. Inability to open the eyelids is not an acceptable reason. If you cannot assess the eye, discuss with ophthalmology. Gross examination of the eyelids, conjunctiva, sclera, cornea, and anterior chamber may reveal lacerations, anatomic disruption, haemorrhage, or foreign bodies. Contact lenses and superficial foreign bodies should also be removed. If a penetrating injury to the eye is suspected, pressure should be avoided.
The eyelids and periocular region should be inspected, taking note of asymmetry, oedema, ecchymosis, lacerations, foreign bodies, or abnormal eyelid position. Any ‘black eye’ with a sharply defined border should be regarded as a sign of an underlying fracture (Figure 9.1).
Ptosis (drooping of the upper eyelid) is common following injury and is typically the result of oedema. Other causes include third nerve palsy, levator muscle injury, or traumatic Horner’s syndrome. Medial eyelid lacerations should raise the suspicion of canalicular injury. The presence of fatty tissue within a lid laceration indicates perforation of the orbital septum and should raise suspicion for an orbital injury, globe injury, and a foreign body. The orbital rims should be palpated for bony steps and tenderness. Any sensory loss in the cheek and forehead should be noted and compared to the other side. Periorbital surgical emphysema is highly suggestive of a fracture involving the cheek, orbital floor, or medial orbital wall. When the nose is blown, air normally contained within the sinuses escapes into the soft tissue. It can also occur in some infections or any erosive pathology that destroys bone. The intercanthal distance has a wide range; in Caucasians, for example, it is about 28–35 mm. Increased intercanthal distance >40 mm (approximately the width of the patient’s eye) suggests displacement of the medial canthal tendon. These patients require CT imaging (see Chapter 7).
This should be determined independently in each eye using a Snellen chart, with the patient wearing their spectacles or using a pinhole. Topical anaesthetics may help if the patient has acute pain or blepharospasm. If unable to visualize print, record counting fingers at a specified distance, hand motion, light perception, or no perception.
Pupil size and reactivity are important determinants of globes status, particularly in the unconscious. The size, shape, symmetry, and reaction to light should be noted. Patients should also be assessed for a relative afferent pupillary defect (RAPD).
Globe position and ocular motility
The presence of proptosis and dystopia should be noted. This may indicate haemorrhage, infection, inflammation, or tumour. Looking at the orbits from above (bird’s-eye view) or below (worm’s-eye view) assists in determining the degree of proptosis. Reflection of light off the patient’s corneas should be in the same position in both eyes. This means that the globes are level and looking in the same direction. If one eye appears lower than the other this is called hypoglobus, or vertical ocular dystopia. This may be seen in zygomatic or orbital floor fractures, or space-occupying lesions or swellings. If the eye appears ‘sunken in’ this is likely to be enophthalmos, indicating an orbital fracture. Be careful, the globe may also appear sunken in if it is ruptured or is a prosthesis. Proptosis (exophthalmos) is common, but usually mild following injury. Remember non-traumatic causes as well.
The patient should be able to painlessly move their eyes in all directions. Limited motility has many causes (notably fractures, muscle injury, entrapment, cranial nerve injury, or orbital oedema and blood). When assessing eye movements, move the object slowly—otherwise subtle restriction may be overlooked. Look closely as they look up. If there is entrapment the axis of rotation shifts and sometimes the eye can be seen to rotate into the orbit. This is called a ‘retraction sign’.
It is important to distinguish whether diplopia is monocular or binocular. Diplopia that persists when the opposite eye is covered is monocular and suggests an abnormality of the globe, such as corneal irregularity, lens abnormality or iridodialysis. Diplopia that resolves when covering either eye is a defect in the coordinated eye movement. Diplopia on upward gaze is a clinical sign of orbital floor entrapment whereas in downward gaze it can be associated with dysfunction of the inferior rectus from simple bruising.
Visual field testing can detect a number of disorders. Confrontational (face-to-face) visual field assessments are measured one eye at a time and can be performed by comparing the patient’s fields to the examiner’s own field (assuming that the examiner has normal visual fields). At a normal conversational distance, a target (e.g. fingers or cotton-tipped applicators) can be placed at the periphery of the visual field equidistant between the examiner and patient. Care must be taken to ensure that the unexamined eye of the patient is completely covered.
Intraocular pressure measurement
Elevated intraocular pressure (IOP) can result from numerous conditions, including hyphaema, glaucoma, RBH, tumours, thyroid eye disease, or carotid-cavernous fistula. Decreased IOP can result from open-globe injury, uveitis, cyclodialysis (separation of the ciliary body from the sclera), or retinal detachment. IOP may be measured using an applanation tonometer, portable Tono-Pen®, or Schiotz tonometer. Topical anaesthesia (tetracaine) is necessary.
See also Chapter 10.
A FBC with differential is usually required for any infective, inflammatory, systemic, or neoplastic pathologies.
The ESR should be taken when symptoms suggest the possibility of temporal arteritis.
Occipitomental (15 and 30 degrees) and lateral facial views are commonly required in the preliminary assessment of zygomatic/orbital and some mid-face injuries. They are also of use in the preliminary assessment of the maxillary and ethmoid sinuses.
Soft tissue views may be required to locate a foreign body.
CT has largely replaced conventional plain film radiography in the evaluation of periorbital trauma and other sinus/orbital pathology (tumours, infections, etc.). CT is particularly useful in the evaluation of orbital fractures, intraocular and orbital foreign bodies, globe rupture, and space-occupying lesions. However, radiolucent foreign bodies such as plastic or wood may be difficult to detect on CT or plain film. Standard CT examination should include both axial and coronal views. Sagittal views are also very useful in the evaluation of orbital floor injuries. With today’s modern scanners all these views are now easily obtained. Contrast is not necessary in trauma, but may be for other pathologies, so the patient’s U&Es may need to be checked. MRI is useful in the evaluation of suspected tumours or soft tissue abnormalities.
This may be required urgently following trauma (especially penetrating injuries). If bleeding is active, selective embolization may be necessary. Angiography is also occasionally undertaken in the assessment of vascular swellings (alternatively, CTA or MRA may be performed).
Orbital fractures (isolated)
Orbital fractures can affect any of the orbital walls or orbital margin. These may occur in isolation or be part of a larger fracture complex, with involvement of the surrounding bones (e.g. NOE, zygomatic, anterior cranial fossa). The term ‘blowout’ fracture refers specifically to an isolated injury to one or more orbital walls (commonly the floor or medial wall) but with the surrounding orbital rims intact. The orbital floor and medial orbital wall are particularly delicate and are easily damaged, resulting in these fractures. There are two proposed mechanisms. A direct blow to the globe (e.g. squash ball to the eye) can result in the transfer of energy directly to the orbital floor or medial wall. In these cases the globe can also be seriously injured. Alternatively, a blow to the prominence of the cheek, can deform the bone such that it ‘buckles’, resulting in fracture propagation within the orbit. This type of fracture may be associated with concurrent facial fractures to the zygoma or mid face.
• Swelling/bruising/tenderness (not specific)
• Diplopia (usually on looking up) (Figure 9.2)
• Enophthalmos/vertical ocular dystopia
• Proptosis may occur if there is a lot of swelling or surgical emphysema
• Numbness of the cheek
• Globe injury.
• Occipitomental and lateral facial views (for associated cheek or mid-facial injury) may suggest a ‘hanging drop’ sign. This may represent the herniation of orbital contents into the maxillary sinus. However, it may not be easily seen and not all ‘hanging drops’ are herniated contents. Nevertheless, it is an important sign and merits further investigation. A fluid level in the sinus suggests there is a fracture somewhere.
• Coronal/axial CT of orbits.
• Orthoptic assessment—Hess chart, measurement of globe projection and fields of binocular vision (to assess restriction of ocular movement). Swelling may preclude immediate assessment.
In all cases it is important to advise the patient not to blow their nose. This is because if they do, pressurized air can pass through the nose and antrum (sinus) into the orbit via the fracture. This potentially could introduce bacteria and result in orbital cellulitis. See Figure 9.3.
Many hospitals advise prophylactic antibiotics specifically. Initial measures include:
• Tell patient not to blow their nose for 3 weeks.
• If they have to sneeze, do so with mouth open.
• Consider antibiotics (co-amoxiclav 375 mg three times daily for 5 days).
• Tell the patient to return if they have increasing swelling, pain, or change in visual acuity.
• Chloramphenicol ointment may be applied to any conjunctival injury.
• Refer to maxillofacial surgery, or specialty that repairs facial fractures.
• If there are ocular symptoms, refer also to ophthalmology.
Never allow a patient with a suspected blowout fracture to go home if you have been unable to assess the eye. Inability to open the eyelids is not an acceptable reason. If you cannot assess the eye, discuss with ophthalmology.
Surgical repair of a blowout fracture is not necessary in every case and is not urgent, except in children where it can be a surgical emergency. The eye takes priority. Where an injury to the globe or associated nerves is suspected, an ophthalmic opinion should be sought.
• Significant diplopia
• A retraction sign
• Dystopia (displacement of globe)
• A ‘large’ blowout on CT—said to predispose to the late development of enophthalmos.
The aim of repair is to release entrapped soft tissues and restore orbital geometry and volume. This should release any restrictions on eye movement and restore globe position. Timing of surgery is controversial and dependent on multiple factors. If the tissues are very swollen or there are minimal signs it is common practice to delay surgery for up to 10–14 days post-injury. This allows any swelling to settle and gives an idea of any disability.
In children, the orbits are shallow and there is a greater chance of muscle entrapment and ischaemic incarceration of the orbital soft tissues or muscles. Inappropriate pain, blepharospasm, or vomiting may suggest this. Immediate surgical intervention is indicated.
Cheek fractures are common injuries and comprise a spectrum from relatively simple fractures resulting in minimal cosmetic problems, to complex patterns causing gross disfigurement and considerable functional disability. The terminology can also be a little confusing as they often go by a variety of names (zygoma, malar, zygomaticomaxillary, tripod—to name a few!).
The typical fracture pattern is that of a tetrapod. The ‘feet’ or ‘pods’ relate to the four main sites of fracture displacement, which can be identified either clinically or radiographically. The arch fractures separately from the remaining sites, which are joined together by a continuous ring of interlinking fractures. Together this allows separation of the entire cheek from the rest of the facial skeleton. Although commonly seen ‘en bloc’, as the energy transfer increases from mild to moderate to severe, fracture complexity increases correspondingly, with progression to comminution. Management can therefore vary widely. From a practical viewpoint fractures can be considered as:
• Zygomatic arch
• Infraorbital rim (uncommon)
• Minimally displaced
• Significantly displaced
• Fractures with associated mid-facial or complex orbital floor/wall injury.
All zygomaticomaxillary fractures, by definition, have a fracture line running through the orbit. Patients should therefore be assessed for ocular injury, diplopia, and entrapment. The eye takes priority. Associated ocular problems include:
• Globe/muscle injury
• Superior orbital fissure syndrome
• Orbital apex syndrome.
These vary depending on the force of impact and degree of displacement of the cheek. They include:
• Signs of injury:
• Subconjunctival haemorrhage
• Surgical emphysema
• Signs of orbital involvement:
• Double vision/limitation of eye movement
• Proptosis (exophthalmos)
• Signs of fracture displacement:
• Flattening of the malar prominence (often masked by swelling immediately after injury)
• Palpable infraorbital step
• Antimongoloid slant
• Hypoglobus (vertical ocular dystopia)
• Altered sensation of cheek/upper lip
• Malocclusion (premature contact of the molar teeth on the side of injury).
A well-defined ‘black eye’ or a subconjunctival haematoma with no posterior limit, are reliable signs of a fracture involving the orbit. Assess these patients carefully.
• Visual acuity/orthoptic assessment.
• Occipitomental, lateral face. Look carefully, sometimes the only clue is a fluid level in the antrum.
• CT scan.
• Ultrasound scan and maxillary sinus endoscopy for orbital floor fractures have been reported as useful techniques but usually have no role in an emergency department setting. They are rarely undertaken.
Interpreting occipitomental views
To the inexperienced, interpreting occipitomental images can be tricky. This is probably due to a combination of complex anatomy, superimposition of the skull (notably vascular markings and sutures), and the relatively oddly angled views compared with images taken elsewhere in the body. The best way to learn is to see plenty of examples. A number of useful approaches have been described to help in interpretation. See Figures 9.4 and 9.5.
Knowledge of a ‘tetrapod’ fracture configuration enables one to inspect the key areas (or ‘pods’) on an occipitomental view. These are the sites where displacement is most noticeable. Alternatively the ‘baby elephant’ interpretation involves checking the sites shown (one infraorbital rim, two frontozygomatic sutures, and three zygomaticomaxillary buttress) and looking for a broken ‘trunk’!
In all cases it is important to advise the patient not to blow their nose. This is because if they do, pressurized air can pass through the nose and antrum into the orbit via the fracture. This potentially could introduce bacteria and result in orbital cellulitis. Many hospitals advise prophylactic antibiotics specifically. Initial measures include:
• Tell patient not to blow their nose for 3 weeks.
• If they have to sneeze, do so with mouth open.
• Consider antibiotics (co-amoxiclav 375 mg three times daily for 5 days).
• Chloramphenicol ointment may be applied to any conjunctival injury.
• Refer to maxillofacial surgery, or specialty that repairs facial fractures
• If there are ocular symptoms, refer also to ophthalmology.
Never allow a patient with a suspected zygomatic fracture to go home if you have been unable to assess the eye. Inability to open the eyelids is not an acceptable reason. If you cannot assess the eye, discuss with ophthalmology.
Surgery is usually carried out either immediately or about 5–6 days following injury. Many fractures are treated by open reduction and internal fixation (ORIF) with titanium miniplates. Surgical access for reduction and fixation is commonly through the mouth to avoid facial scars. Access to the frontozygomatic suture and infraorbital rim may also be necessary to assist reduction and fixation.
The bulging eye (proptosis/exophthalmos)
Proptosis, or exophthalmos, is the forward displacement of the eye in the orbit. Since the orbit is essentially a closed cavity, any enlargement of structures located within it will cause this. It can be unilateral or bilateral, acute or longstanding. When unilateral and non-traumatic, consider an orbital tumour or orbital cellulitis. Some degree of proptosis, usually minor, is common following trauma to the eye or orbit. Complete or partial dislocation of the globe from the orbit is possible but is very rare. In the vast majority of cases proptosis is not vision threatening despite its obvious cosmetic effects. Nevertheless, many patients complain of symptoms related to a dry eye and if the cornea remains unprotected serious complications can occur.
All cases of proptosis should be investigated for underlying or associated pathology (notably thyroid disease or orbital tumour).
• Periorbital trauma (from retrobulbar swelling, bleeding, displaced bones/air)
• Graves’ ophthalmopathy (hyperthyroidism). This can also cause unilateral proptosis
• Orbital cellulitis
• Orbital pseudotumour
• High-altitude cerebral oedema
• Wegener’s granulomatosis
• Tumours (leukaemia, lymphoma, meningioma, sarcoma, etc.)
• Dermoid cyst
• Carotid-cavernous fistula (look for pulsation)
• High myopia (short-sightedness).
Proptosis following trauma occurs in approximately 3% of craniofacial injuries. However, vision-threatening proptosis is a much rarer event. Nevertheless, when it occurs urgent intervention is required if loss of vision is to be prevented. Usually proptosis is apparent by the time the patient arrives in the emergency department, but delayed presentation of up to several days can also occur.
The orbit is essentially a rigid box, except anteriorly. It is therefore at risk of a compartment syndrome following trauma. Bleeding or swelling quickly results in a rapid rise in interstitial pressure, decreased perfusion pressure, and, if untreated, ischaemia and infarction. Re-establishment of perfusion is therefore essential if sight is to be saved. The two most common causes of sight-threatening proptosis following trauma are gross swelling behind the eye (orbital compartment syndrome (OCS)) and bleeding behind the eye (RBH).
Retrobulbar haemorrhage/orbital compartment syndrome
RBH is usually a clinical diagnosis and needs to be treated as soon as possible. It is effectively an acute compartment syndrome within the orbit and should be managed with the same degree of urgency as compartment syndromes elsewhere in the body. Raised intra-orbital pressure is caused by bleeding and oedema. This is contained within the bony orbit, behind the relatively unyielding orbital septum. Bleeding can occur within or outside the muscle ‘cone’, formed by the recti muscles, intra-conal bleeding being more severe. As the pressure rises, it compresses the ophthalmic and retinal vessels, resulting in retinal and optic ischaemia. In many cases there is no bleeding but oedema. When severe enough, this presents in exactly the same way. This is termed orbital compartment syndrome (OCS).
Consider retrobulbar haemorrhage if there is:
• Severe eye pain
• Acute proptosis
• Visual loss/RAPD
• Severely decreased eye movements in all directions (ophthalmoplegia).
Marked lid oedema may make proptosis difficult to recognize. Inability to open the eyelids with any one of these features is highly suspicious for RBH/OCS. Failure to recognize this may result in blindness. Irreversible damage has been estimated to occur following only 90 minutes of ischaemia. Raised IOP can be assessed with a Tono-Pen®, however many emergency departments will not have this equipment available. Therefore if suspected it is better to err on the side of caution and assume it is present. Time is of the essence in any patient with deteriorating vision and increasing pain—these are the ones in whom treatment is most likely to be successful. If you can, perform an immediate lateral canthotomy and cantholysis. If you cannot, get immediate help and learn how to do this. As for a surgical airway, this needs to be done immediately and any delay waiting for a ‘specialist’ to arrive will worsen the prognosis. Urgent referral to ophthalmology and maxillofacial surgery is also required (depending on local referral pathways). The canthotomy just buys time. Formal decompression may be required, depending on the clinical picture.
Lateral canthotomy with lateral canthal tendon division can be performed under local anaesthesia in the emergency department. Lignocaine 1% with adrenaline (epinephrine) (1 in 200,000) is injected into the lateral canthal area of the affected eye and the lateral canthus is incised to the orbital rim and the identified canthal tendon cut. The tendon is identified by ‘strumming’ the tissues, while the eyelid is pulled medially and out. Great care must be taken to avoid damage to the globe. The lower lid attachment is always divided and some authorities recommend division of the upper lid attachment as well. This allows the globe to translate forward, partially relieving the pressure by effectively increasing the retrobulbar volume. The steps for this are:
• Clean the site with sterile saline.
• Inject local anaesthetic into the lateral canthus.
• Crush the lateral canthus with a straight haemostat, advancing the jaws of the clip into the lateral fornix until the rim of the bony orbit is felt.
• Clamp for 30–60 seconds.
• Using straight scissors, make a 1 cm long horizontal incision of the lateral canthal tendon, in the middle of the crush mark.
• Grasp the lower eyelid with toothed forceps, pulling the eyelid away from the face. This pulls the inferior crus (the band of the lateral canthal tendon) tight so it can be easily cut loose from the orbital rim. It will have a ‘banjo string’ feel against the tip of the scissors.
• Continue to pull the lower eyelid outwards and downwards away from the eye.
• Use blunt-tipped scissors to cut the inferior crus.
• Keep the scissors parallel (flat) to the face with the tips pointed towards the chin. Place the inner blade just anterior to the conjunctiva and the outer blade just deep to the skin.
• The globe should pull freely away. It may also ‘pop’ forward, relieving the pressure. Cut any residual lateral attachments of the lower eyelid if it does not move freely.
• Do not worry about cutting ½ cm of conjunctiva or skin. The lower eyelid is cut, relieving orbital pressure.
• If the intact cornea is exposed apply ointment or lubricant to prevent corneal desiccation and infection.
•Do not apply absorbent gauze dressing to the exposed cornea.
See Figure 9.6.
This should be commenced in addition to the canthotomy.
• Mannitol (osmotic diuretic) 20% 2 g/kg IV over 5 minutes.
• Dexamethasone 8 mg IV.
• Acetazolamide (carbonic anhydrase inhibitor, reduces production of aqueous humour), 500 mg IV then 250 mg 6-hourly for 24 hours.
Visual acuity is the key to urgency. If the vision is normal, patients can be investigated urgently to find the precise cause. But if the vision is rapidly deteriorating, or already significantly affected, time is of the essence. Think of the vision as the ‘GCS of the eye’.
Assessment of proptosis in the unconscious patient
Comprehensive assessment of proptosis in the emergency department, ICU, or operating theatre is usually not possible in the early stages of management. What is possible is often limited, even more so if the patient is confused, agitated, or unresponsive. Differentiation between RBH and OCS on clinical grounds alone is not always possible since both share similar features.
In awake patients, clinical urgency can be determined by deterioration in visual acuity. However, in the unconscious or agitated patient, this is not possible. Pain and ophthalmoplegia, two further indicators of vision-threatening proptosis, also cannot be determined. It is also worth remembering that a well-made prosthetic eye can fool all but the most astute of clinicians. In unconscious patients, initial assessment of any proptosis is therefore significantly restricted to a relatively crude examination. This includes assessment of the eyelids, pupils, careful palpation of the globes, and, if possible, fundoscopy (or portable slit lamp examination). Each has its limitations. In many patients, the only readily identifiable signs of RBH/OCS will be a ‘tense’, proptosed globe with an abnormally reacting pupil and swollen disc. The main issue is to maintain a high index of suspicion and to seek advice early.
If the patient requires a CT scan of part of their body and their condition allows, request a CT of the orbits (or head). The additional time required to obtain these scans is now relatively small and you may identify a treatable cause of proptosis.
Remember that proptosis following trauma has several causes:
• Blood (RBH)
• Oedema (OCS)
• Air (surgical emphysema)
• Bone (fractures displaced into the orbit)
• Brain (craniofacial fractures)
• Contrast material (interventional radiology), a rare cause.
This is a severe infection deep to the orbital septum, involving the orbital contents. The commonest source of infection is from infected periorbital sinuses (especially the ethmoid), or from spread of a preseptal cellulitis. The orbital septum is therefore a key anatomical landmark, which acts as a barrier to spread of infection during the initial stages. Tooth abscesses and organisms introduced by trauma are other, less common causes.
Patients with orbital cellulitis are often unwell with a high fever and a painful, swollen eye. There is a quick onset of rapidly worsening symptoms often with a history of sinus disease, periorbital infection, or injury. There is marked proptosis, chemosis, and lid oedema, which is red, hot, and tender to touch. Visual acuity and colour vision are reduced, together with an RAPD, if the optic nerve is involved. Eye movements are reduced and painful. Fundoscopy may show swollen optic nerve head and artery or vein occlusions.
The main differential diagnosis is pre-septal cellulitis, which is less severe and represents an infection anterior to the septum. This generally follows an eyelid infection. If there is blurred vision, or the conjunctiva is injected, even without other signs of posterior involvement, assume orbital cellulitis until proven otherwise.
• Patients should be urgently admitted. Refer to ophthalmology.
• FBC, biochemistry, and blood cultures should be performed.
• CT of the orbit and brain is necessary to look for intracranial involvement, pus, and to assess the sinuses.
• Commonly associated pathogens are Staphylococcus aureus, Streptococcus pneumoniae and pyogenes, and (in children) Hamophilus influenzae. High-dose, broad-spectrum IV antibiotics that cover both anaerobic and aerobic organisms should be administered after the blood cultures have been taken. Metronidazole and ceftazidime is one such combination.
• Urgent surgical drainage of orbital, sinus, tooth, and brain abscesses is usually required.
The prognosis is good if treated early. Optic neuropathy and vascular occlusions carry poor visual prognosis. Cavernous sinus thrombosis has poor prognosis (see Chapter 3).
In children, a rhabdomyosarcoma can mimic orbital cellulitis.
Orbital cellulitis can lead to meningitis, brain abscess, cavernous sinus thrombosis, septic shock, and death. It is vital for it to be diagnosed and managed promptly.
Sinusitis may present in many ways and may be confused with atypical facial pain, dental infections, orbital infections, osteomyelitis, or a tumour. The majority of infections are related to an initial rhinitis (as rhinosinusitis), but some can arise secondarily to dental infections in the upper teeth. Untreated sinusitis can spread to involve all four sinuses (maxillary, ethmoid, frontal, and sphenoid) sometimes referred to as pansinusitis. This is a potentially life- and sight-threatening condition. See Figure 9.7.
Sinusitis often arises following an URTI. Blockage of the draining ostia, paralysis of the cilia, and stagnation of secretions within the sinus predisposes to superadded infection. Any sinus can be affected, but the maxillary and ethmoid sinuses are the more common. Dental infections involving the upper teeth can also cause maxillary sinusitis. The roots of the molar and premolar teeth are sometimes separated from the sinus mucosa only by ‘wafer-thin’ bone, or dehisced bone. Infection within the pulp chamber can therefore pass through the tip (apex) of the root into the sinus relatively easily. The absence of toothache does not rule out dental causes.
Acute maxillary sinusitis
This is commonly caused by upper respiratory commensals (pneumococci, staphylococci, streptococci, and anaerobes), or untreated upper dental infections. There is often some predisposing obstruction to the opening of the middle meatus, preventing the sinus from draining freely. This results in stagnation and then infection.
Clinically there is:
• Systemic upset
• Severe cheek pain, worse on bending
• Swelling over the cheek
• Numbness of the cheek
• Mobile upper teeth, which are tender to percussion (in severe cases).
Patients usually present with unilateral swelling of the face, sometimes referred to as a ‘fat face’. Untreated, sinusitis can result in bacteraemia, or even septicaemia. The latter can occasionally lead to septic shock.
Usually the FBC will show an increased WCC. Blood cultures and a raised ESR may indicate the presence of bacteraemia or septicaemia. Radiographically there is radio-opacity of the involved sinus on an occipitomental view. CT scan is required to assess the extent of infection. Infected large dental cysts should also be considered. If these are not identified a sinus washout will not remove all the pus.
Closure of the eyelids from swelling should be taken seriously—the eye should be assessed and the patient often needs to be admitted.
Chronic maxillary sinusitis
An underlying cause should be considered (dental disease, cystic fibrosis, or Kartagener’s syndrome). Symptoms are similar to the acute infection but much less in severity. CT and MRI scans are useful diagnostic tests, although a high percentage of asymptomatic people have ‘abnormal’ scans. Diagnosis and treatment is therefore on clinical grounds.
Acute frontal sinusitis
(See Chapter 3.) This is potentially serious due to the risk of intracranial infection. Patients complain of frontal headache, which is tender to percussion. Untreated, the infection can spread intracranially or involve the orbit.
Acute ethmoid sinusitis
(See Chapter 7.) This usually occurs in association with other sinus infections. Patients complain of deep-seated pain and throbbing deep to the bridge of the nose. The medial orbital walls are paper thin, so orbital cellulitis can rapidly develop.
Management of sinusitis
Antibiotics and, in some cases, sinus washout with drainage using functional endoscopic sinus surgery. Ephedrine nasal drops and menthol inhalations may help reduce congestion and improve sinus drainage. Consider screening for diabetes and other causes of immunosuppression. Symptoms requiring urgent assessment or referral include:
These patients probably need to be admitted for IV antibiotics and close observation.
Thyroid eye disease
Thyroid eye disease (TED) is frequently termed Graves’ ophthalmopathy and is part of an autoimmune process that can affect the orbital and periorbital tissue, the thyroid gland (hyperthyroidism), and rarely pre tibial skin. An antibody-mediated reaction with lymphocytic infiltration of the orbital tissues results in an increase in volume of the orbital contents. This involves both the extraocular muscles and fat. This can cause bilateral or unilateral proptosis. Patients present with irritation around the eye, painful eye movements, a red eye, and, if severe, decreased vision. There is lid retraction, proptosis, chemosis, periorbital oedema, and altered ocular mobility. Initially an acute or subacute stage can make the differential diagnosis of orbital cellulitis difficult. In the latter there is usually a fever. Untreated, TED can cause vision-threatening exposure keratopathy, diplopia, and compressive optic neuropathy. Look for systemic features of hyperthyroidism. TED can also occur in euthyroid state. Investigations include thyroid function tests (thyroid-stimulating hormone, T3, and T4 levels) and thyroid autoantibodies.
Ocular irritation without inflammation can be managed with artificial tear supplements. Mild ocular surface inflammation can be managed with topical steroids. Acute severe TED that can compromise optic nerve function should be referred urgently to ophthalmology urgently for management with IV methylprednisolone. Surgical decompression of the orbits is rarely indicated acutely.
Diplopia (double vision)
Diplopia occurs when one or both eyes are either moved out of alignment (by displacement of a fracture or by an orbital mass/swelling), or they lose their ability to move precisely together (either because of nerve/muscle weakness, or mechanical restriction). This is called binocular diplopia. Less commonly, diplopia may occur secondary to a problem within just one of the globes. This is called monocular diplopia.
Binocular diplopia is a common complaint following injuries to the orbit/eye, but in most cases it is temporary and secondary to swelling/bruising around the extraocular eye muscles. Nevertheless, it can also be a symptom of significant orbital or globe injury, and in some cases requires surgical repair (see ‘Orbital fractures (isolated)’, pp. [link]–[link]). Diplopia can also occur in other non-traumatic conditions, notably tumours, and therefore needs careful evaluation.
Causes of diplopia
These include ophthalmologic, traumatic, infectious, autoimmune, neurological, and neoplastic causes:
• Alcohol intoxication
• Fractures to the zygoma/orbit/NOE/skull
• CN III, IV, VI injury
• Orbital/extraocular eye muscles, swelling/bruising
• Orbital myositis
• Neurological disease (MS)
• Orbital abscess
• Graves’ disease
• Globe disorders.
In gross cases, confirmation of diplopia may be possible by clinical examination of eye movements and looking at the corneal light reflex. However, in more subtle cases diplopia may only be apparent at the extremes of eye moments. All cases require an orthoptic assessment.
Diplopia associated with proptosis is worrying and requires an urgent CT (to look for a space-occupying orbital lesion). Other investigations are guided by the history (notably of trauma, or the presence of visual impairment, and/or pain). Progressive, persistent, or significant diplopia requires urgent referral to either ophthalmology or maxillofacial, depending on local protocol.