Orbits Flashcards
What are the structures making up the roof of the orbit?
The lesser wing of the sphenoid
and the orbital plate of the frontal bone.
What might a defect in the orbital roof cause?
pulsatile proptosis due to transmission of cerebrospinal fluid pulsation to the orbit.
What are the structures making up the lateral wall of the orbit?
the greater wing of the sphenoid and the zygomatic.
What are the structures making up the floor of the orbit?
three bones: the zygomatic, maxillary and palatine.
What are the structures making up the medial wall of the orbit?
four bones: maxillary, lacrimal,
ethmoid and sphenoid. The lamina papyracea, which forms
part of the medial wall, is paper-thin and perforated by numerous foramina for nerves and blood vessels
What sinusitis is orbital cellulitis most likely secondary to?
ethmoidal sinusitis due to paper thin wall and orbital connection
What structures pass through the SOF?
○ The superior portion contains the lacrimal, frontal and trochlear nerves and the superior ophthalmic vein.
○ The inferior portion contains the superior and inferior divisions of the oculomotor nerve, the abducens and nasociliary nerves and sympathetic fibres from the cavernous plexus.
What is Tolosa-Hunt syndrome?
Inflammation of the superior orbital fissure and apex (Tolosa–Hunt syndrome) may therefore result in a multitude of signs including ophthalmoplegia and venous
outflow obstruction
What structures pass through the IOF?
the maxillary nerve, the zygomatic nerve and branches of the
pterygopalatine ganglion, as well as the inferior ophthalmic vein.
What is the length of the intraorbital portion of the optic nerve?
25mm
What conditions cause axial proptosis?
space-occupying lesions within the muscle cone such as a cavernous haemangioma or optic nerve tumours
cause axial proptosis
What conditions cause proptosis and dystopia?
extraconal lesions
What is dystopia?
displacement of the globe in the coronal plane, usually due to an extraconal orbital mass such as a
lacrimal gland tumour
What measurements on exophthalmometry indicate exophthalmos?
20mm or more or a difference between the 2 eyes 2-3mm
What are the causes of pseudoproptosis?
(the false impression of proptosis) may be due to facial asymmetry, enlargement of the globe (e.g.
high myopia or buphthalmos), lid retraction or contralateral
enophthalmos.
What is enophthalmos and list some causes?
implies recession of the globe within the orbit. Causes include congenital and traumatic orbital wall abnormali-
ties, atrophy of the orbital contents (e.g. radiotherapy, scleroderma,
chronic eye poking in blind infants – the ‘oculodigital’ sign) or
sclerosis (e.g. metastatic scirrhous carcinoma, sclerosing orbital
inflammatory disease).
What tests can differentiate a restrictive from neurological motility defect?
Forced duction test
Differential IOP test
Saccadic eye movements
What is the forced duction test?
Under topical anaesthesia, the insertion of the muscle in an involved eye is grasped with forceps and the
globe rotated in the direction of reduced mobility. Checked
movement of the globe indicates a restrictive problem. No resistance will be encountered with a neurological lesion.
What is the differential IOP test?
The IOP is measured in the primary position of gaze and then with the patient attempting to look in
the direction of limited mobility. An increase of 6 mmHg or more denotes resistance transmitted to the globe by muscle restriction (the Braley sign).
What is the saccadic eye movements test?
in neurological lesions are reduced
in velocity, while restrictive defects manifest normal saccadic velocity with sudden halting of ocular movement.
What is a bruit?
a sign found with a larger carotid–cavernous fistula. It is best heard with the bell of the stethoscope and is lessened or abolished by gently compressing the ipsilateral carotid
artery in the neck
What is a pulsation?
caused either by an arteriovenous communication or a defect in the orbital roof. In the former, pulsation
may be associated with a bruit depending on the size of the
communication. In the latter the pulsation is transmitted from
the brain by the cerebrospinal fluid and there is no associated
bruit. Mild pulsation is best detected on the slit lamp, particularly by applanation tonometry.
What is optic atrophy?
may be preceded by swelling,
is a feature of severe compressive optic neuropathy. Important
causes include thyroid eye disease and optic nerve tumours.
What are opticociliary collaterals?
consist of enlarged pre-existing peri-
papillary capillaries that divert blood from the central retinal venous circulation to the peripapillary choroidal circulation when there is obstruction of the normal drainage channels
The collaterals may be associated with any orbital or optic nerve tumour that compresses the intraorbital optic nerve and impairs blood flow through the central retinal vein. The most common tumour associated with shunts is an optic nerve sheath meningioma but they may also occur with optic nerve glioma, central retinal vein occlusion, idiopathic intracranial hypertension and glaucoma.
What is Orbital CT good for?
1) Depicting bony structures
2) Location and size of space-occupying lesions.
3) Small fractures
4) Foreign bodies
5) Blood
6) Herniation of EOM and emphysema
7) Confirm an orbital abscess
What is MRI orbits good for?
1) Orbital apex lesions
2) Intracranial extension of tumours
3) Useful for monitoring inflammatory disease
4) STIR scans for TED
What tumour does opticociliary shunt vessels on the disc commonly represent?
Optic nerve sheath meningioma
What is the pathophysiology of Graves disease?
an autoimmune disorder
in which IgG antibodies bind to thyroid stimulating hormone
(TSH) receptors in the thyroid gland and stimulate secretion of
thyroid hormones.
What is the major risk factor to develop TED once a patient has Graves disease?
Smoking
What can radioactive iodine do to TED?
Worsen it
What is the pathophyisology of TED?
Organ-specific autoimmune
reaction in which an antibody that reacts against thyroid gland cells and orbital fibroblasts leads to inflammation of extraocular muscles, interstitial tissues, orbital fat and lacrimal glands characterized by pleomorphic cellular infiltration, associated with increased secretion of glycosaminoglycans and osmotic imbibition of water.
There is an increase in the volume of the orbital contents, particularly the muscles, which can swell to eight times their normal size. There may be a secondary elevation of intraorbital
pressure, and the optic nerve may be compressed. Subsequent degeneration of muscle fibres eventually leads to fibrosis, which exerts a tethering effect on the involved muscle, resulting in
restrictive myopathy and diplopia
Stages of TED?
Congestive (Inflammatory) stage in which eyes are red and painful. Remits in 1-3 years. Only 10% develop serious long term problems
Quiescent stage in which eyes white but painless motility defect may be present
What are some clinical features of TED?
(i) soft tissue involvement,
(ii) lid retraction,
(iii) proptosis,
(iv) optic neuropathy
(v) restrictive myopathy.
What is the EUGOGO classification and elaborate on it?
1) sight-threatening due to optic neuropathy or corneal breakdown;
2) moderate–severe, with one of moderate–severe soft tissue involvement, lid retraction of 2 mm or more, diplopia and proptosis of 3 mm or more;
3) mild, with only a minor impact on
daily life.
What is lid retraction?
Retraction of upper and lower lids occurs in about 50% of patients
with Graves disease. Overaction of Müller muscle is postulated to
occur as a result of sympathetic overstimulation secondary to high
levels of thyroid hormones.
What is Dalrymple sign?
moderate bilateral asymmetrical lid retraction
What is Kocher sign?
severe bilateral lid retraction
What is von-Graefe sign?
lid lag on downgaze
What % of TED patients develop ophthalmoplegia which may be permanent?
Between 30% and 50% of patients
Motility defects in the order of frequency in TED?
○ Elevation defect caused by fibrotic contracture of the inferior rectus, may mimic superior rectus palsy and
is the most common motility deficit.
○ Abduction defect due to fibrosis of the medial rectus, which may simulate sixth nerve palsy.
○ Depression defect secondary to fibrosis of the superior rectus.
○ Adduction defect caused by fibrosis of the lateral rectus.
What % of patients with TED get optic neuropathy?
(up to 6%)
Does proptosis need to be present for optic nerve compression?
compression of the optic nerve
secondary to enlarged and congested rectus muscles may occur in the absence of proptosis.
How to assess for optic neuropathy in TED?
○ Visual acuity (VA) is usually reduced, but not invariably.
○ Colour desaturation is a sensitive feature.
○ There may be diminished light brightness appreciation.
○ A relative afferent pupillary defect, if present, should give cause for marked concern.
○ Visual field defects can be central or paracentral and may be combined with nerve fibre bundle defects. These findings, in concert with elevated IOP, may be confused with primary open-angle glaucoma.
○ The optic disc may be normal, swollen or, rarely, atrophic.
How to manage mild TED?
○ Lubricants for SLK, corneal exposure and dryness.
○ Topical anti-inflammatory agents (steroids, (NSAIDs), ciclosporin) are advocated by some authorities.
○ Head elevation with three pillows during sleep to reduce periorbital oedema.
○ Eyelid taping during sleep may alleviate mild exposure keratopathy.
How to manage moderate TED?
○ Systemic steroids are the mainstay of treatment for moderate–severe disease. Oral prednisolone 60–80 mg/day may be given initially and tapered depending on response.
Intravenous methylprednisolone is often reserved for acute compressive optic neuropathy, but tolerability is better, and outcomes may be superior, compared with oral treatment.
A lower-intensity regimen
in the absence of acute sight-threatening disease is 0.5 g once weekly for 6 weeks followed by 0.25 g once weekly for 6 weeks. A reduction in discomfort, chemosis and periorbital oedema usually occurs within 24 hours, with a maximal response within 2–8 weeks. Ideally, oral steroid therapy should be discontinued after several months, but long-term low-dose maintenance may be necessary.
○Orbital steroid injections are occasionally used in selected cases to minimize systemic side effects, but are typically considerably less effective than systemic treatment.
○ Low-dose fractionated radiotherapy. A positive response is usually evident within 6 weeks, with maximal improvement by 4 months; around 40% will not respond.
○Combined therapy with irradiation, azathioprine and low-
dose prednisolone may be more effective than steroids or
radiotherapy alone.
When is orbital wall decompression useful in TED?
if steroids are ineffective (20% receiving intravenous treatment) or
contraindicated. Orbital radiotherapy may also be administered, but is generally only used as an adjunct to other modalities.
What steroid regimen is a good idea for Optic neuropathy?
Pulsed intravenous methylprednisolone is commonly used, regimens including 0.5–1 g on 3 successive days with conversion to
oral treatment (e.g. 40 mg/day prednisolone) or 0.5–1 g
on alternate days, 3–6 times, keeping the maximum dose below 8 g to reduce the risk of liver compromise, followed by oral prednisolone.
What monoclonal disease modifying drug is useful in TED?
monoclonal antibody treatment with rituximab and teprotumumab. Teprotumumab is an inhibitor of insulin-like growth factor 1 receptor (IGF-1R) and is effective in reducing proptosis and the Clinical Activity Score in patients with TED.
How can the proptosis be treated once the inflammation has remitted in TED?
the patient can be left with cosmetically and functionally
significant proptosis, the treatment of which is essentially surgical. Surgical decompression increases the volume
of the orbit by removing the bony walls and may be combined with removal of orbital fat.
How many walls are decompressed in TED proptosis?
Most surgery is undertaken via an external approach, though the medial
wall and the medial part of the floor can be reached endoscopically. One-wall (deep lateral) decompression is
effective (approximately 4–5 mm reduction in proptosis) and may reduce the risk of postoperative diplopia
Two-wall (balanced medial and lateral) decompression provides a greater effect but with a significant risk of inducing diplopia
Three-wall decompression includes the floor with a reduction in proptosis of 6–10 mm but may lead to hypoglobus and carries a higher risk of infraorbital nerve damage and diplopia. Very severe proptosis may
require removal of part of the orbital roof in addition (four-wall decompression).
When is surgery for restrictive myopia performed in TED?
provided the inflammatory stage has
subsided and the angle of deviation has been stable for at least 6–12 months.
What type of muscle surgery is commonly performed in TED?
Recession of the inferior and/or medial recti is the most commonly indicated surgery (a rectus muscle is never resected, only recessed
in TED), generally utilizing adjustable sutures .
The suture is adjusted later the same day or on the first postoperative day to achieve optimal alignment and the
patient is encouraged subsequently to practise achieving single vision with a consistently accessible target such as a television.
How can lid retraction be treated in TED?
1) Mild lid retraction frequently improves spontaneously
2) Control of hyperthyroidism
3) Botulinum toxin injection to the levator aponeurosis and Müller
muscle may be used as a temporary measure in patients awaiting definitive correction.
What organisms are typically responsible for preseptal cellulitis?
Staphylococcus aureus and Streptococcus pyogenes,
Difference between preseptal and orbital cellulitis
in contrast to orbital cellulitis, proptosis and chemosis are absent and VA, pupillary reactions and ocular motility are unimpaired. The
patient is often pyrexial.
Treatment for preseptal cellulitis?
oral antibiotics such as co-amoxiclav
250–500 mg/125 mg 2–3 times daily or 875/125 mg twice daily,
depending on severity. Severe infection may require intravenous antibiotics. The patient’s tetanus status should be ascertained in
cases following trauma.
Which pathogens cause orbital cellulitis?
Streptococcus pneumoniae, Staphylococcus aureus,
Streptococcus pyogenes
and Haemophilus influenzae
How does orbital cellulitis actually happen?
infection originating typically from the paranasal (especially ethmoid) sinuses. Infection can also spread from preseptal cellulitis, dacryocystitis, midfacial skin or dental infection and can follow trauma, including any form of ocular surgery. Blood-borne spread from infection elsewhere in the body may occur
Differential diagnoses for orbital cellulitis?
Infection
*Bacterial orbital cellulitis
*Fungal orbital infection
*Dacryocystitis
*Infective dacryoadenitis
Vascular lesions
*Acute orbital haemorrhage
*Cavernous sinus thrombosis
*Carotid–cavernous fistula Neoplasia
*Rapidly progressive retinoblastoma
*Lacrimal gland tumour
*Other neoplasm, e.g. metastatic lesion with inflammation, lymphoma, Waldenström macroglobulinaemia
*Rhabdomyosarcoma, leukaemia, lymphangioma or neuroblastoma in children
Endocrine
*Thyroid eye disease of rapid onset
Non-neoplastic inflammation
*Idiopathic orbital inflammatory disease
*Tolosa–Hunt syndrome
*Orbital myositis
*Acute allergic conjunctivitis with lid swelling
*Herpes zoster ophthalmicus
*Herpes simplex skin rash
*Sarcoidosis
*Vasculitides: granulomatosis with polyangiitis, polyarteritis nodosa
*Scleritis, including posterior scleritis
*Ruptured dermoid cyst
How to investigate orbital cellulitis?
*Ascertainment of tetanus immunization status in cases of
trauma.
*White cell count.
*Blood cultures.
*Culture of nasal discharge.
*High-resolution CT of the orbit, sinuses and brain is vital to confirm the diagnosis and exclude a subperiosteal or intracranial abscess. MRI is also sometimes performed.
*Lumbar puncture if meningeal or cerebral signs develop.
How to treat orbital cellulitis?
*Hospital admission is mandatory, with urgent ENT assessment and frequent ophthalmic review.
Paediatric specialist advice should be sought in the management of
a child and a low threshold should be adopted for infectious disease specialist consultation.
* Delineation of the extent of erythema on the skin using a
surgical marker may help in judging progress.
* Antibiotics are given intravenously, with the specific drug depending on local sensitivities. Ceftazidime is a typical choice, supplemented by oral metronidazole to cover anaerobes. Intravenous antibiotics should be continued until the patient has been apyrexial for 4 days, followed by 1–3 weeks of oral treatment.
What is Rhino-orbital Mucormycosis and which population of people does it tend to affect?
a rare aggressive and often fatal infection caused by fungi of the family Mucoraceae. It typically affects patients with diabetic ketoacidosis or immunosuppression and is extremely rare in the immunocompetent
How does rhino-orbital mucormycosis spread to the orbits?
Infection is acquired by the inhalation
of spores, which give rise to an upper respiratory infection. Spread then occurs to the contiguous sinuses and subsequently to the orbit and brain. Invasion of blood vessels by the hyphae results in occlusive vasculitis with infarction of orbital tissues.
How to investigate rhino-orbital mucormycosis
*Ascertainment of tetanus immunization status in cases of
trauma.
*White cell count.
*Blood cultures.
*Culture of nasal discharge.
*High-resolution CT of the orbit, sinuses and brain is vital to confirm the diagnosis and exclude a subperiosteal or intracranial abscess. MRI is also sometimes performed.
*Lumbar puncture if meningeal or cerebral signs develop.
What are some symptoms and signs of rhino-orbital mucormycosis
- Symptoms. Gradual onset facial and periorbital swelling, diplopia and visual loss.
- Signs are similar to bacterial orbital cellulitis, but tend to be less acute and with slower progression. Infarction superimposed on septic necrosis is responsible for the classic black eschar that may develop on the palate, turbinates, nasal septum, skin
and eyelids
What is the treatment for rhino-orbital mucormycosis
- Correction of the underlying metabolic defect should be instituted if possible.
- Intravenous antifungal treatment.
- Daily packing and irrigation of the involved areas with anti-
fungal agent. - Wide excision of devitalized and necrotic tissues. Exenteration
may be required in unresponsive cases in order to reduce the
risk of death. - Adjunctive hyperbaric oxygen may be helpful.
Histopathological diagnosis of NSOI/orbital pseudotumour?
pleomorphic inflammatory cellular infiltration followed by reactive fibrosis.
What are some symptoms and signs of NSOI?
acute or subacute ocular and
periocular redness, swelling and pain
*Signs
○ Pyrexia is present in up to 50% of children, but is rare in adults.
○ Congestive proptosis.
○ Mild to severe ophthalmoplegia may occur.
○ Features of optic nerve dysfunction, particularly if the inflammation involves the posterior orbit. There may be optic disc swelling.
○ Choroidal folds, if present, may be associated with reduced vision but optic neuropathy must always be suspected.
What is the course of NSOI?
Variable
○ Spontaneous remission after a few weeks without sequelae.
○ Intermittent episodes of activity, usually with eventual remission.
○ Severe prolonged inflammation eventually leading to progressive fibrosis of orbital tissues, resulting in a ‘frozen orbit’ characterized by ophthalmoplegia, which may be
associated with ptosis and visual impairment caused by optic nerve involvement.
How to investigate NSOI?
○CT shows ill-defined orbital opacification and loss of
definition of contents
○Biopsy is generally required in persistent cases to confirm
the diagnosis and particularly to rule out neoplasia and systemic inflammatory conditions.
○A wide range of other investigations may be considered to aid in the exclusion of alternative diagnoses, particularly infection, lymphoma and non-neoplastic infiltrative disorders such as sarcoidosis and Wegener granulomatosis.
How to treat NSOI?
- Observation, for relatively mild disease, in anticipation of
spontaneous remission.
*NSAIDs alone (e.g. ibuprofen) are often effective and may be tried in mild disease prior to steroid therapy. Co-prescription of a proton pump inhibitor should be considered.
*Systemic steroids should be administered only after the
diagnosis has been confirmed, as they may mask other pathology such as infection and Wegener granulomatosis. Oral prednisolone is initially given at a dose of 1.0–1.5 mg/kg/day, subsequently being tapered and discontinued over a number of weeks depending on clinical response.
*Radiotherapy may be considered if there has been no improvement after 2 weeks of adequate steroid therapy.
What is orbital myositis and what does histology show?
an idiopathic, non-specific inflammation of one or more extraocular muscles and is considered a subtype of IOID. Histology shows a chronic inflammatory cellular infiltrate
associated with the muscle fibres
What are some symptoms and signs of Orbital myositis?
*Symptoms. Acute pain, exacerbated by eye movement and diplopia. Onset is usually in early adulthood.
*Signs are generally less obvious than NSOI
○Lid oedema, ptosis and chemosis.
○Pain and diplopia associated with eye movements.
○Vascular injection over the involved muscle
○In chronic cases fibrosis of the affected muscle may occur with permanent restrictive myopathy.
What is the course of Orbital myositis?
○Acute non-recurrent involvement that resolves spontaneously within 6 weeks.
○Chronic disease characterized by either a single episode persisting for longer than 2 months (often for years) or recurrent attacks.
How is orbital myositis investigated?
primarily of MRI or CT, which show
enlargement of the affected muscles, with or without involvement of the tendons of insertion. This is in
contrast to TED-related muscle enlargement, in which the tendon is always spared. Additional investigations may be required in some cases.
How is orbital myositis treated?
Treatment is aimed at relieving discomfort and dysfunction,
shortening the course and preventing recurrences. NSAIDs may be adequate in mild disease, but systemic steroids are generally required and usually produce dramatic improvement, although recurrence is seen in 50%. Radiotherapy is also effective, particularly in limiting recurrence.
What are the causes of acute dacryoadenitis?
idiopathic or due to viral (e.g. mumps, Epstein–Barr, cytomegalovirus) or – rarely – bacterial infection
How does acute dacryoadenitis present?
There is tenderness over the lacrimal gland and injection of the conjunctiva overlying the palpebral lobe may be
seen on upper lid eversion
