Thyrotoxicosis
🔸 Graves disease, the most common form of hyperthyroidism.It is more common in females
🔸
Presentation is often in the fourth or fifth decades
Symptoms:
including weight loss despite good appetite, increased bowel frequency, sweating, heat
🔸
intolerance, nervousness, irritability, palpitations, weakness and fatigue.
Signs:
including enlargement of the thyroid gland, tremor, palmar erythema, and warm and sweaty skin.
🔸
Cardiac manifestations may include sinus tachycardia and other arrhythmias.
Risk factors for ophthalmopathy :
Once a patient has Graves disease, the major clinical risk factor for developing TED are:
-smoking.
-Women are five times more likely to be affected .
-Radioactive iodine used to treat hyperthyroidism can worsen TED.
🔸 Pathogenesis of ophthalmopathy:
an 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 , 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 intra orbital
pressure, and the optic nerve may be compressed. Subsequent degeneration of muscle fibers
eventually leads to fibrosis, resulting in restrictive myopathy and diplopia.
🔷 Optic nerve glioma 🔶 ii-Lid retraction:
Retraction of upper and lower lids occurs in about 50% of patients with Graves
- Typically affects children
🔹
- Has a very poor prognosis if occurs in adult males.
🔶
🔸 i-Soft tissue involvement:
disease. Over action of Müller muscle as a result of sympathetic over stimulation ,
🔹Symptoms: Slowly progressive visual loss, followed later by proptosis. Fibrotic contracture of the levator palpebrae and inferior rectus muscles associated
Signs: Proptosis is often non-axialThe optic nerve head, initially swollen, Symptoms: Grittiness, red eyes, lacrimation, photophobia, puffy lids and with adhesion to overlying orbital tissues is another probable mechanism.
subsequently becomes atrophic.Opticociliary collaterals and other fundus signs
such as central retinal vein occlusion are occasionally seen.Intracranial spread to 🔸
retrobulbar discomfort.
Signs: Epibulbar hyperaemia, Periorbital swelling is caused by oedema and
infiltration behind the orbital septum , chemosis and prolapse of retroseptal fat into
Symptoms: Patients may complain of bulging eyed appearance, difficulty closing
the eyes and ocular surface symptoms.
🔹
the chiasm and hypothalamus may develop. Signs: -The Dalrymple sign is lid retraction in primary gaze.-The Kocher sign
Investigation : MRI, CT in patients with associated NF1 shows a fusiform the eyelids, Tear insufficiency and instability, Corneal signs are exacerbated by lid describes a staring and frightened appearance of the eyes which is particularly
retraction and include punctate epithelial erosions, superior limbic keratoconjunctivitis
🔹
enlargement of the optic nerve marked on attentive fixation.-The von Graefe sign signifies retarded descent of the
Treatment: As the tumour is intrinsic to the optic nerve, resection means that all and occasionally bacterial keratitis, thinning and scarring upper lid on downgaze
vision will be lost in the operated eye.
🔷 RHABDOMYOSARCOMA 🔷 Optic nerve sheath meningioma
A benign tumour arising from meningothelial cells.Typically affect middle-aged women.The
NEURAL TUMOURS
- The most common primary orbital malignancy in children Clinical features:
🔹
- 40% develop in the head and neck
🔹
prognosis for life is good in adults, although the tumour may be more aggressive in children
THYROID EYE DISEASE TED typically proceeds through 🔶 iv-Restrictive myopathy :
🔹Symptoms: Rapidly progressive unilateral proptosis.
Signs: The tumour is most commonly superonasal or superior, but may arise anywhere 🔹 Symptoms: gradual visual impairment in one eye.
Signs: The classic triad consists of progressive visual loss, optic atrophy and opticociliary A congestive (inflammatory) stage in which the eyes are red and painful: this tends to
remit within 1–3 years and only about 10% of patients develop serious long term ocular
Between 30% and 50% of patients with TED develop ophthalmoplegiaand this may
🔹
in the orbit, including inferiorly. shunt vessels.Restrictive motility defects, particularly in upgaze.Proptosis. be permanent.Ocular motility is restricted initially by inflammatory oedema, and
problems.
🔹Investigation:
It can also arise in other tissues, such as conjunctiva and uvea. Swelling and redness of MRI, CT shows thickening and calcification of the optic nerve. later by fibrosis.
A fibrotic stage follows in which the eyes are white, although a painless motility defect may Symptoms. Double vision, and often discomfort in some positions of gaze.Muscles
🔹 🔶
overlying skin develop but the skin is not warm .Diplopia is frequentpain is less common. Treatment: not be indicated in a middle-aged patient with a slowly growing lesion, but
excision is required for an aggressive tumour. radiotherapy may be appropriate as a vision- be present. involved are inferior rectus causing elevation defect, medial rectus with Abduction
Treatment: a combination of radiotherapy, chemotherapy and sometimes surgical Clinical features can be categorized into : iii-Proptosis:
debulking. The prognosis for patients with disease confined to the orbit isgood. sparing approach, or as adjunctive treatment following surgery is axial, unilateral or bilateral, symmetrical or defect , superior rectus with Depression defect and lateral rectus with Adduction
(i) soft tissue involvement defect.
(ii) lid retraction asymmetrical and frequently permanent.
(iii) proptosis Severe proptosis may compromise lid closure
(iv) optic neuropathy and along with lid retraction and tear
(v) restrictive myopathy dysfunction can lead to exposure keratopathy,
corneal ulceration and infection.
🔶 v-Optic neuropathy :
serious complication caused by compression of the optic nerve or its blood supply
at the orbital apex by the congested and enlarged recti Ms and swollen orbital
🔷 Preseptal cellulitis
An infection of the subcutaneous tissues anterior to the orbital septum.More common than
tissue.
-Symptoms: Impairment of central vision .
-Signs : Visual acuity (VA) is usually reduced, Colour desaturation is a sensitive
orbital cellulitis, and less serious.Rapid progression to orbital cellulitis may occasionally occur. feature, diminished light brightness appreciation , A relative afferent pupillary
Organisms typically responsible are Staphylococcus aureus and Streptococcus pyogenes. defect, Visual field defects can be central or paracentral , The optic disc may be
Causes : skin trauma such as laceration or insect bites, spread from focal ocular or periocular normal, swollen or, rarely, atrophic.
infection such as an acute hordeolum, dacryocystitis, conjunctivitis or sinusitis, and
haematogenous spread from remote infection such as the upper respiratory tract or middle
ear. 🔷 Treatment:
Stop smoking, Thyroid dysfunction should also be managed adequately,if radioiodine treatment is administered in
Post-inflammatory complications. Eyelid surgery should be performed only after any
necessary orbital and then strabismus procedures have been undertaken, as orbital
Manifests with a swollen, often firm, tender red eyelid . decompression may impact both ocular motility and eyelid position, and extraocular muscle
🔹
patients with pre-existing TED, a short course of oral steroids should be given.
Treatment is with oral antibiotics. surgery may affect eyelid position.Proptosis. the treatment of which is surgical. Surgical
i-Mild disease
-Lubricants for superior limbic keratoconjunctivitis, corneal exposure and dryness. decompression increases the volume of the orbit by removing the bony walls and may be
-Topical anti-inflammatory agents (steroids, non-steroidal anti-inflammatory drugs (NSAIDs),and ciclosporin) . combined with removal of orbital fat.Restrictive myopathy. Surgery is required in most cases
-Head elevation with three pillows during sleep to reduce periorbital oedema. experiencing persistent diplopia in the primary or reading positions of gaze , provided the
-Eyelid taping during sleep may alleviate mild exposure keratopathy inflammatory stage has subsided and the angle of deviation has been stable for at least 6–12
months. Until these criteria are met, diplopia may be alleviated, if possible, with prisms or
🔹 ii-Moderate to severe active disease
-Systemic steroids , Oral prednisolone 60–80 mg/ day may be given initially, and tapered depending on response.
sometimes botulinum toxin.
Lid retraction. Mild lid retraction frequently improves spontaneously so does not require
-Orbital steroid injections are occasionally used in selected cases to minimize systemic side effects, but are typically
🔷 Bacterial orbital cellulitis
A serious infection of the soft tissues behind the orbital septum
considerably less effective than systemic treatment.
-Radiotherapy may be used in addition to steroids or when steroids are contraindicated or ineffective, Adverse effects
treatment. Control of hyperthyroidism may also be beneficial. Botulinum toxin injection to the
levator aponeurosis and Müller muscle may be used as a temporary measure in patients
awaiting definitive correction. Müllerotomy (disinsertion of Müller muscle) is effective for mild
Sight- and life-threatening include cataract, radiation retinopathy, optic neuropathy and an increased risk of local cancer.
lid retraction, but more severe cases may also require recession/disinsertion of the levator
-Combined therapy with irradiation, azathioprine and low-dose prednisolone may be more effective than steroids or
🔹
occurs at any age but is more common in children aponeurosis and the suspensory ligament of the superior conjunctival fornix. Recession of the
radiotherapy alone.Optic neuropathy, requires aggressive treatment. Intravenous methylprednisolone , followed by oral
Organisms : Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes and Haemophilus prednisolone
lowerlid retractors, used when retraction of the lower lid is 2 mm or more
🔹
influenzae
Causes :
🔷 Rhino-orbital mucormycosis
infection originating from the :paranasal (especially ethmoid) sinuses.preseptal cellulitis Dacryocystitismidfacial skin or
dental infection and trauma, including any form of ocular surgery. Blood-borne spread from infection elsewhere in the
INFECTIONS Orbit
A rare aggressive and often fatal infection caused by fungi of the family Mucoraceae.
body may occur. Idiopathic orbital inflammatory Disease
Affects patients with diabetic ketoacidosis or immunosuppression.
Infection is acquired by the inhalation of spores, which give rise to an upper respiratory infection.
🔹 Symptoms :
rapid onset of pain exacerbated by eye movement, swelling of the eye, malaise, and frequently visual impairment and
- Orbital pseudotumour
- Non-neoplastic, non-infective, space occupying orbital infiltration with inflammatory features.
Spread then occurs to the sinuses and to the orbit and brain. - Involve any or all of the orbital soft tissues.
🔹Pyrexia,
double vision. There is commonly a recent history of nasal, sinus or respiratory symptoms. - Histopathology: pleomorphic inflammatory cellular infiltration followed by reactive fibrosis.
Invasion of blood vessels by the hyphae results in occlusive vasculitis with infarction of orbital
tissues. Signs: - Unilateral disease is typical in adults, although in children bilateral involvement may occur.
🔹
VA may be reduced and colour vision impaired, raisingthe possibility of optic nerve compression; the presenceof
🔹 Symptoms: a relative afferent pupillary defect , Tender, firm, erythematous and warm eyelids, with periocular and conjunctival
(chemosis) oedema,conjunctival injection and sometimes subconjunctival haemorrhage; the signs are usually unilateral,
Symptoms :
🔹
Gradual onset facial and periorbital swelling, diplopia and visual loss. Acute or subacute ocular and periocular redness, swelling and pain. systemic symptoms are common in
though oedema may spread to the contralateral eyelids.
🔹
Signs: children.
Similar to bacterial orbital cellulitis, but tend to be less acute and with slower progression. Infarction Proptosis is common . it may be non-axial (dystopia), particularly if an abscess is present. Painful ophthalmoplegia. Signs
superimposed on septic necrosis is responsible for the classic black scar that may develop on the
🔷
🔹
- Pyrexia is present in up to 50% of children, but is rare in adults.
🔹
palate, turbinates, nasal septum, skin and eyelids. Complications: - Congestive proptosis.
Complications :Retinal vascular occlusionMultiple cranial nerve palsies Cerebrovascular Ocular complications - Mild to severe ophthalmoplegia .
occlusion. Optic neuropathy - optic nerve dysfunction.
🔹 Treatment
-Correction of the underlying metabolic defect should be instituted if possible.
Exposure keratopathy
Raised IOP 🔹
- Choroidal folds associated with reduced vision.
Course:
Endophthalmitis The natural history of the inflammatory process is very variable.
-Intravenous antifungal treatment. Occlusion of the central retinal artery or vein. - Spontaneous remission after a few weeks without sequelae.
🔹
-Daily packing and irrigation of the involved areas with antifungal agent. Subperiosteal abscess, most frequently located along the medial orbital wall.
-Wide excision of devitalized and necrotic tissues - Intermittent episodes of activity, usually with eventual remission.
Intracranial complications, uncommon (3–4%) but extremely serious, include: MeningitisBrain abscess Cavernous - Severe prolonged inflammation eventually leading to progressive fibrosis of orbital tissues, resulting in a
-Exenteration required in unresponsive cases in order to reduce the risk of death. sinus thrombosis.
-Adjunctive hyperbaric oxygen may be helpful. ‘frozen orbit’ characterized by ophthalmoplegia, which may be associated with ptosis and visual
🔷 Treatment
Hospital admission
impairment caused by optic nerve involvement.
🔹Investigation- CT shows ill-defined orbital opacification and loss of definition of contents- Biopsy
🔹
Antibiotics are given intravenously
Monitoring of optic nerve function is performed at least every 4 hours initially by testing: -VA-colour vision-light Treatment
brightness appreciation -pupillary reactionsDeterioration should prompt the consideration of surgical intervention.. Observation, for relatively mild disease
Surgery: Drainage of an orbital abscess ; drainage of infected sinuses , Severe optic nerve compression may warrant an NSAIDs alone (e.g. ibuprofen) in mild disease prior to steroid therapy.Systemic steroids
emergency canthotomy/cantholysis. Orbital steroid injection may be useful in some cases.
Radiotherapy may be considered if there has been no improvement after 2 weeks of adequate steroid
therapy.In resistant cases, include cytotoxic drugs (e.g. methotrexate, azathioprine)
Surgical resection of an inflammatory focus in highly resistant cases
🔶 Acute dacryoadenitis
🔶 Cavernous sinus thrombosis 🔶 Orbital myositisI
Idiopathic or due to viral (e.g. mumps, Epstein–Barr, cytomegalovirus) or – rarely – bacterial infection.
Chronic conditions such as sarcoidosis, Sjögren syndrome, thyroid disease and some chronic infections
Resulting from infection such as sinusitis, orbital or preseptal NON-INFECTIVE diopathic, non-specific inflammation of one or more extraocular muscles and is
🔸
usually give a less acute onset, and involvement can be bilateral.
🔸
cellulitisor otitis. considered a subtype of IOID. Presentation
-mortality rate: 20% in treated pt. INFLAMMATORYDISEASES Symptoms: rapid onset of discomfort in the region of the gland. Lacrimal secretion may be reduced or increased,
🔸
-mortality rate: up to 100% in untreated pt. Acute pain, exacerbated by eye movement, and diplopia; onset is usually in early and discharge may be reported.
NON-NEOPLASTIC
🔸
Features are of rapid onset and may include severe adulthood. Swelling of the lateral aspect of the eyelid overlying the palpebral lobe leads to a characteristic S-
headachemalaise, nausea and vomitingProptosis ,unilateral or often Signs: shaped ptosis enlargement of the orbital lobe may give a slight downward and inward dystopia
bilateral chemosis, congestion of the facial, conjunctival and retinal VASCULARABNORMALITIES Lid oedema, ptosis and chemosis.Pain and diplopia associated with eye proptosis and other signs of orbital disease.
🔸
veins, reduced vision movements.Vascular injection over the involved muscleIn chronic cases the affected tenderness over the lacrimal gland Chemosis and injection of the conjunctiva local (e.g. pre-auricular)
🔸
🔸
signs resulting from compromised function of the third to sixth muscle become fibrosed, with permanent restrictive myopathy. lymph node enlargement.
🔸
cranial nerves, which run through the cavernous sinus.
Treatment consists of intravenous antibiotics and sometimes
surgical drainage.
Treatment:
NSAIDs in mild diseasesystemic steroids produce dramatic improvement.
Treatment:
varies according to the cause, but in many cases is not required.
Radiotherapy in limiting recurrence.
by fatema okoff
🔶 Tolosa–Hunt syndrome
A rare idiopathic condition caused by non-specific granulomatous inflammation
of the cavernous sinus, superior orbital fissure and/or orbital apex. It is a diagnosis
🔸
of exclusion
Presentation, ipsilateral :periorbital or hemicranial paindiplopia due to one or
more ocular motor paresespupillary and eyelid involvement in many cases.
Proptosis is mildSensory loss along the distribution of the first and second divisions
🔸
of the trigeminal nerve is commonThe patient may be pyrexial.
Treatmentis with systemic steroids and other immunosuppressants
🔸 Graves disease, the most common form of hyperthyroidism.It is more common in females
🔸
Presentation is often in the fourth or fifth decades
Symptoms:
including weight loss despite good appetite, increased bowel frequency, sweating, heat
🔸
intolerance, nervousness, irritability, palpitations, weakness and fatigue.
Signs:
including enlargement of the thyroid gland, tremor, palmar erythema, and warm and sweaty skin.
🔸
Cardiac manifestations may include sinus tachycardia and other arrhythmias.
Risk factors for ophthalmopathy :
Once a patient has Graves disease, the major clinical risk factor for developing TED are:
-smoking.
-Women are five times more likely to be affected .
-Radioactive iodine used to treat hyperthyroidism can worsen TED.
🔸 Pathogenesis of ophthalmopathy:
an 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 , 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 intra orbital
pressure, and the optic nerve may be compressed. Subsequent degeneration of muscle fibers
eventually leads to fibrosis, resulting in restrictive myopathy and diplopia.
🔷 Optic nerve glioma 🔶 ii-Lid retraction:
Retraction of upper and lower lids occurs in about 50% of patients with Graves
- Typically affects children
🔹
- Has a very poor prognosis if occurs in adult males.
🔶
🔸 i-Soft tissue involvement:
disease. Over action of Müller muscle as a result of sympathetic over stimulation ,
🔹Symptoms: Slowly progressive visual loss, followed later by proptosis. Fibrotic contracture of the levator palpebrae and inferior rectus muscles associated
Signs: Proptosis is often non-axialThe optic nerve head, initially swollen, Symptoms: Grittiness, red eyes, lacrimation, photophobia, puffy lids and with adhesion to overlying orbital tissues is another probable mechanism.
subsequently becomes atrophic.Opticociliary collaterals and other fundus signs
such as central retinal vein occlusion are occasionally seen.Intracranial spread to 🔸
retrobulbar discomfort.
Signs: Epibulbar hyperaemia, Periorbital swelling is caused by oedema and
infiltration behind the orbital septum , chemosis and prolapse of retroseptal fat into
Symptoms: Patients may complain of bulging eyed appearance, difficulty closing
the eyes and ocular surface symptoms.
🔹
the chiasm and hypothalamus may develop. Signs: -The Dalrymple sign is lid retraction in primary gaze.-The Kocher sign
Investigation : MRI, CT in patients with associated NF1 shows a fusiform the eyelids, Tear insufficiency and instability, Corneal signs are exacerbated by lid describes a staring and frightened appearance of the eyes which is particularly
retraction and include punctate epithelial erosions, superior limbic keratoconjunctivitis
🔹
enlargement of the optic nerve marked on attentive fixation.-The von Graefe sign signifies retarded descent of the
Treatment: As the tumour is intrinsic to the optic nerve, resection means that all and occasionally bacterial keratitis, thinning and scarring upper lid on downgaze
vision will be lost in the operated eye.
🔷 RHABDOMYOSARCOMA 🔷 Optic nerve sheath meningioma
A benign tumour arising from meningothelial cells.Typically affect middle-aged women.The
NEURAL TUMOURS
- The most common primary orbital malignancy in children Clinical features:
🔹
- 40% develop in the head and neck
🔹
prognosis for life is good in adults, although the tumour may be more aggressive in children
THYROID EYE DISEASE TED typically proceeds through 🔶 iv-Restrictive myopathy :
🔹Symptoms: Rapidly progressive unilateral proptosis.
Signs: The tumour is most commonly superonasal or superior, but may arise anywhere 🔹 Symptoms: gradual visual impairment in one eye.
Signs: The classic triad consists of progressive visual loss, optic atrophy and opticociliary A congestive (inflammatory) stage in which the eyes are red and painful: this tends to
remit within 1–3 years and only about 10% of patients develop serious long term ocular
Between 30% and 50% of patients with TED develop ophthalmoplegiaand this may
🔹
in the orbit, including inferiorly. shunt vessels.Restrictive motility defects, particularly in upgaze.Proptosis. be permanent.Ocular motility is restricted initially by inflammatory oedema, and
problems.
🔹Investigation:
It can also arise in other tissues, such as conjunctiva and uvea. Swelling and redness of MRI, CT shows thickening and calcification of the optic nerve. later by fibrosis.
A fibrotic stage follows in which the eyes are white, although a painless motility defect may Symptoms. Double vision, and often discomfort in some positions of gaze.Muscles
🔹 🔶
overlying skin develop but the skin is not warm .Diplopia is frequentpain is less common. Treatment: not be indicated in a middle-aged patient with a slowly growing lesion, but
excision is required for an aggressive tumour. radiotherapy may be appropriate as a vision- be present. involved are inferior rectus causing elevation defect, medial rectus with Abduction
Treatment: a combination of radiotherapy, chemotherapy and sometimes surgical Clinical features can be categorized into : iii-Proptosis:
debulking. The prognosis for patients with disease confined to the orbit isgood. sparing approach, or as adjunctive treatment following surgery is axial, unilateral or bilateral, symmetrical or defect , superior rectus with Depression defect and lateral rectus with Adduction
(i) soft tissue involvement defect.
(ii) lid retraction asymmetrical and frequently permanent.
(iii) proptosis Severe proptosis may compromise lid closure
(iv) optic neuropathy and along with lid retraction and tear
(v) restrictive myopathy dysfunction can lead to exposure keratopathy,
corneal ulceration and infection.
🔶 v-Optic neuropathy :
serious complication caused by compression of the optic nerve or its blood supply
at the orbital apex by the congested and enlarged recti Ms and swollen orbital
🔷 Preseptal cellulitis
An infection of the subcutaneous tissues anterior to the orbital septum.More common than
tissue.
-Symptoms: Impairment of central vision .
-Signs : Visual acuity (VA) is usually reduced, Colour desaturation is a sensitive
orbital cellulitis, and less serious.Rapid progression to orbital cellulitis may occasionally occur. feature, diminished light brightness appreciation , A relative afferent pupillary
Organisms typically responsible are Staphylococcus aureus and Streptococcus pyogenes. defect, Visual field defects can be central or paracentral , The optic disc may be
Causes : skin trauma such as laceration or insect bites, spread from focal ocular or periocular normal, swollen or, rarely, atrophic.
infection such as an acute hordeolum, dacryocystitis, conjunctivitis or sinusitis, and
haematogenous spread from remote infection such as the upper respiratory tract or middle
ear. 🔷 Treatment:
Stop smoking, Thyroid dysfunction should also be managed adequately,if radioiodine treatment is administered in
Post-inflammatory complications. Eyelid surgery should be performed only after any
necessary orbital and then strabismus procedures have been undertaken, as orbital
Manifests with a swollen, often firm, tender red eyelid . decompression may impact both ocular motility and eyelid position, and extraocular muscle
🔹
patients with pre-existing TED, a short course of oral steroids should be given.
Treatment is with oral antibiotics. surgery may affect eyelid position.Proptosis. the treatment of which is surgical. Surgical
i-Mild disease
-Lubricants for superior limbic keratoconjunctivitis, corneal exposure and dryness. decompression increases the volume of the orbit by removing the bony walls and may be
-Topical anti-inflammatory agents (steroids, non-steroidal anti-inflammatory drugs (NSAIDs),and ciclosporin) . combined with removal of orbital fat.Restrictive myopathy. Surgery is required in most cases
-Head elevation with three pillows during sleep to reduce periorbital oedema. experiencing persistent diplopia in the primary or reading positions of gaze , provided the
-Eyelid taping during sleep may alleviate mild exposure keratopathy inflammatory stage has subsided and the angle of deviation has been stable for at least 6–12
months. Until these criteria are met, diplopia may be alleviated, if possible, with prisms or
🔹 ii-Moderate to severe active disease
-Systemic steroids , Oral prednisolone 60–80 mg/ day may be given initially, and tapered depending on response.
sometimes botulinum toxin.
Lid retraction. Mild lid retraction frequently improves spontaneously so does not require
-Orbital steroid injections are occasionally used in selected cases to minimize systemic side effects, but are typically
🔷 Bacterial orbital cellulitis
A serious infection of the soft tissues behind the orbital septum
considerably less effective than systemic treatment.
-Radiotherapy may be used in addition to steroids or when steroids are contraindicated or ineffective, Adverse effects
treatment. Control of hyperthyroidism may also be beneficial. Botulinum toxin injection to the
levator aponeurosis and Müller muscle may be used as a temporary measure in patients
awaiting definitive correction. Müllerotomy (disinsertion of Müller muscle) is effective for mild
Sight- and life-threatening include cataract, radiation retinopathy, optic neuropathy and an increased risk of local cancer.
lid retraction, but more severe cases may also require recession/disinsertion of the levator
-Combined therapy with irradiation, azathioprine and low-dose prednisolone may be more effective than steroids or
🔹
occurs at any age but is more common in children aponeurosis and the suspensory ligament of the superior conjunctival fornix. Recession of the
radiotherapy alone.Optic neuropathy, requires aggressive treatment. Intravenous methylprednisolone , followed by oral
Organisms : Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes and Haemophilus prednisolone
lowerlid retractors, used when retraction of the lower lid is 2 mm or more
🔹
influenzae
Causes :
🔷 Rhino-orbital mucormycosis
infection originating from the :paranasal (especially ethmoid) sinuses.preseptal cellulitis Dacryocystitismidfacial skin or
dental infection and trauma, including any form of ocular surgery. Blood-borne spread from infection elsewhere in the
INFECTIONS Orbit
A rare aggressive and often fatal infection caused by fungi of the family Mucoraceae.
body may occur. Idiopathic orbital inflammatory Disease
Affects patients with diabetic ketoacidosis or immunosuppression.
Infection is acquired by the inhalation of spores, which give rise to an upper respiratory infection.
🔹 Symptoms :
rapid onset of pain exacerbated by eye movement, swelling of the eye, malaise, and frequently visual impairment and
- Orbital pseudotumour
- Non-neoplastic, non-infective, space occupying orbital infiltration with inflammatory features.
Spread then occurs to the sinuses and to the orbit and brain. - Involve any or all of the orbital soft tissues.
🔹Pyrexia,
double vision. There is commonly a recent history of nasal, sinus or respiratory symptoms. - Histopathology: pleomorphic inflammatory cellular infiltration followed by reactive fibrosis.
Invasion of blood vessels by the hyphae results in occlusive vasculitis with infarction of orbital
tissues. Signs: - Unilateral disease is typical in adults, although in children bilateral involvement may occur.
🔹
VA may be reduced and colour vision impaired, raisingthe possibility of optic nerve compression; the presenceof
🔹 Symptoms: a relative afferent pupillary defect , Tender, firm, erythematous and warm eyelids, with periocular and conjunctival
(chemosis) oedema,conjunctival injection and sometimes subconjunctival haemorrhage; the signs are usually unilateral,
Symptoms :
🔹
Gradual onset facial and periorbital swelling, diplopia and visual loss. Acute or subacute ocular and periocular redness, swelling and pain. systemic symptoms are common in
though oedema may spread to the contralateral eyelids.
🔹
Signs: children.
Similar to bacterial orbital cellulitis, but tend to be less acute and with slower progression. Infarction Proptosis is common . it may be non-axial (dystopia), particularly if an abscess is present. Painful ophthalmoplegia. Signs
superimposed on septic necrosis is responsible for the classic black scar that may develop on the
🔷
🔹
- Pyrexia is present in up to 50% of children, but is rare in adults.
🔹
palate, turbinates, nasal septum, skin and eyelids. Complications: - Congestive proptosis.
Complications :Retinal vascular occlusionMultiple cranial nerve palsies Cerebrovascular Ocular complications - Mild to severe ophthalmoplegia .
occlusion. Optic neuropathy - optic nerve dysfunction.
🔹 Treatment
-Correction of the underlying metabolic defect should be instituted if possible.
Exposure keratopathy
Raised IOP 🔹
- Choroidal folds associated with reduced vision.
Course:
Endophthalmitis The natural history of the inflammatory process is very variable.
-Intravenous antifungal treatment. Occlusion of the central retinal artery or vein. - Spontaneous remission after a few weeks without sequelae.
🔹
-Daily packing and irrigation of the involved areas with antifungal agent. Subperiosteal abscess, most frequently located along the medial orbital wall.
-Wide excision of devitalized and necrotic tissues - Intermittent episodes of activity, usually with eventual remission.
Intracranial complications, uncommon (3–4%) but extremely serious, include: MeningitisBrain abscess Cavernous - Severe prolonged inflammation eventually leading to progressive fibrosis of orbital tissues, resulting in a
-Exenteration required in unresponsive cases in order to reduce the risk of death. sinus thrombosis.
-Adjunctive hyperbaric oxygen may be helpful. ‘frozen orbit’ characterized by ophthalmoplegia, which may be associated with ptosis and visual
🔷 Treatment
Hospital admission
impairment caused by optic nerve involvement.
🔹Investigation- CT shows ill-defined orbital opacification and loss of definition of contents- Biopsy
🔹
Antibiotics are given intravenously
Monitoring of optic nerve function is performed at least every 4 hours initially by testing: -VA-colour vision-light Treatment
brightness appreciation -pupillary reactionsDeterioration should prompt the consideration of surgical intervention.. Observation, for relatively mild disease
Surgery: Drainage of an orbital abscess ; drainage of infected sinuses , Severe optic nerve compression may warrant an NSAIDs alone (e.g. ibuprofen) in mild disease prior to steroid therapy.Systemic steroids
emergency canthotomy/cantholysis. Orbital steroid injection may be useful in some cases.
Radiotherapy may be considered if there has been no improvement after 2 weeks of adequate steroid
therapy.In resistant cases, include cytotoxic drugs (e.g. methotrexate, azathioprine)
Surgical resection of an inflammatory focus in highly resistant cases
🔶 Acute dacryoadenitis
🔶 Cavernous sinus thrombosis 🔶 Orbital myositisI
Idiopathic or due to viral (e.g. mumps, Epstein–Barr, cytomegalovirus) or – rarely – bacterial infection.
Chronic conditions such as sarcoidosis, Sjögren syndrome, thyroid disease and some chronic infections
Resulting from infection such as sinusitis, orbital or preseptal NON-INFECTIVE diopathic, non-specific inflammation of one or more extraocular muscles and is
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usually give a less acute onset, and involvement can be bilateral.
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cellulitisor otitis. considered a subtype of IOID. Presentation
-mortality rate: 20% in treated pt. INFLAMMATORYDISEASES Symptoms: rapid onset of discomfort in the region of the gland. Lacrimal secretion may be reduced or increased,
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-mortality rate: up to 100% in untreated pt. Acute pain, exacerbated by eye movement, and diplopia; onset is usually in early and discharge may be reported.
NON-NEOPLASTIC
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Features are of rapid onset and may include severe adulthood. Swelling of the lateral aspect of the eyelid overlying the palpebral lobe leads to a characteristic S-
headachemalaise, nausea and vomitingProptosis ,unilateral or often Signs: shaped ptosis enlargement of the orbital lobe may give a slight downward and inward dystopia
bilateral chemosis, congestion of the facial, conjunctival and retinal VASCULARABNORMALITIES Lid oedema, ptosis and chemosis.Pain and diplopia associated with eye proptosis and other signs of orbital disease.
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veins, reduced vision movements.Vascular injection over the involved muscleIn chronic cases the affected tenderness over the lacrimal gland Chemosis and injection of the conjunctiva local (e.g. pre-auricular)
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signs resulting from compromised function of the third to sixth muscle become fibrosed, with permanent restrictive myopathy. lymph node enlargement.
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cranial nerves, which run through the cavernous sinus.
Treatment consists of intravenous antibiotics and sometimes
surgical drainage.
Treatment:
NSAIDs in mild diseasesystemic steroids produce dramatic improvement.
Treatment:
varies according to the cause, but in many cases is not required.
Radiotherapy in limiting recurrence.
by fatema okoff
🔶 Tolosa–Hunt syndrome
A rare idiopathic condition caused by non-specific granulomatous inflammation
of the cavernous sinus, superior orbital fissure and/or orbital apex. It is a diagnosis
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of exclusion
Presentation, ipsilateral :periorbital or hemicranial paindiplopia due to one or
more ocular motor paresespupillary and eyelid involvement in many cases.
Proptosis is mildSensory loss along the distribution of the first and second divisions
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of the trigeminal nerve is commonThe patient may be pyrexial.
Treatmentis with systemic steroids and other immunosuppressants
