This document summarizes various types of orbital inflammation including preseptal cellulitis, orbital cellulitis, idiopathic orbital inflammatory disease, orbital myositis, dacryoadenitis, thyroid orbitopathy, Tolosa-Hunt syndrome, and rhino-orbital mucormycosis. It describes the presentations, risk factors, pathogenesis, diagnostic evaluations, and treatment approaches for each condition. The document emphasizes that orbital inflammatory diseases encompass a broad spectrum and can affect people of all ages, with varying degrees of visual impairment, proptosis, ophthalmoplegia, and pain depending on the specific condition and extent of inflammation present.

1. Orbital Inflammation
Dr Arpita Sthapak

2. Introduction
• Orbital inflammatory diseases encompass a board spectrum of diseases.
• Orbital inflammation accounts for 6% of orbital disease.
• It includes a variety of -
• acute and subacute idiopathic processes
• chronic inflammations
• specific inflammation of uncertain etiology.
• It affects all age group.

3.  Presentations include red eye, proptosis, ophthalmoplegia and
pain.
 In severe cases, the eyeball and optic nerve can be compressed
leading to choroidal folds or compressive optic neuropathy

4. Preseptal cellulitis
 Infection of subcutaneous tissue anterior to orbital septum.
 Causes-
• Skin trauma- laceration or insect bite
the offending organism is s. aureus, or s. pyogenes.
• Spread of local infection- acute hordeolum, dacryocystitis or sinusitis .
• Remote infections- respiratory tract or middle ear by hematogenous
spread.

5. Signs-
• Tender red lid with periorbital edema.
• In contrast to orbital cellulitis proptosis and chemosis are absent, visual
acuity, pupillary reaction and ocular motility are unimpaired

6. Differential diagnosis-
 Orbital cellulitis
 Allergic – sudden onset, non tender itchy , swollen eyelid – contact
dermatitis.
 Cavernous sinus thrombosis.
 Other- insect bite, trauma or maxillary osteomyelitis.
 Treatment – oral co- amoxiclav 500mg every 8 hour, severe
infection require intravenous antibiotics.

7. Opacification anterior
to orbital septum
Left preseptal cellulitis

8. Orbital cellulitis
• It is a life threatening infection of subcutaneous tissue behind the
orbital septum.
• Major cause of orbital cellulitis are:-
 sinusitis(56%)
 lid or face infection(28%)
 foreign body (11%)
 hematogenous(4%)
 Staphylococcus and streptococcus are the most common organism in
adults.
 Haemophilus influenzae in children

9. Epidemiology
 Orbital cellulitis is much less common than preseptal cellulitis .
 Both conditions occur more commonly in the winters as a result of
the increased incidence of paranasal sinus infection.
 There is no predilection for gender .
 Orbital cellulitis is more common in children, and more severe in
diabetics and immunocompromised patients.

10. Presentation- rapid onset of fever, pain and visual impairement.
Signs-
 Unilateral tender, warm and red periorbital and lid oedema.
 Proptosis- lateral and downward.
 Painful ophthalmoplegia
 Optic nerve dysfunction

11. Complications :-
• Ocular –exposure keratopathy
raised intraocular pressure
occlusion of central retinal artery or vein
endophthalmitis
optic neuropathy
• Intracranial – meningitis
brain abscess
cavernous sinus thrombosis

12. Differential diagnosis :-
 preseptal cellulitis
 Chalazion
 Allergic lid swelling
 Cavernous sinus thrombosis
 Other orbital conditions - eg, thyroid eye disease, orbital
tumours/pseudo-tumours, orbital vasculitis
 Other conditions- eg, insect bite, angio-oedema,
maxillary osteomyelitis

13. Investigations -
• Complete blood count,ESR, ANCA
• Blood, nasal, conjunctival and throat culture and sensitivity .
• Ct scan of the orbit and paranasal sinuses to confirm diagnosis
• Rule out retained foreign body, orbital or subperiosteal abscess,
paranasal sinus disease or cavernous sinus thrombosis.

14. • Lumbar puncture if meningeal or cerebral signs present
• Monitoring of optic nerve function- pupillary reaction, colour
vision, visual acuity.

15. Treatment
• Broad spectrum antibiotic
• Nasal decongestant to drain the sinuses.
• Close monitoring by ophthalmologist, neuro surgeon, ENT
surgeon

16.  Antibiotics- All periorbital and orbital infections should be treated
with broad spectrum antibiotics.
 Patients should be treated with parenteral antibiotics until they show
clear evidence of clinical improvement as manifested by a decrease
in orbital congestive signs such as proptosis , gaze limitation and
edema.
 In children less than 4 years of age-
ticarcilline –clavulanic acid 200-300 mg/kg/day
cefotaxime 80-120mg/kg/day in four divided dose
cefuroxime 75-150mg/kg/day in three divided dose.
 In adults- ceftriaxone 1-2 g/day

17. Surgical intervention-in which infected sinuses and orbital collections are
drained ,should be considered in following conditions-
 Suspicion of orbital abscess or foreign body
 Progression of visual loss
 Extraocular motility deficit
 Worsening proptosis despite appropriate medical treatment after 24-48
hours.
 Size of orbital abscess does not reduce on ct scan within 48-72 hours
after treatment.

18. Rhino-orbital mucormycosis
• Mucormycosis are a group of invasive infections which are caused by
filamentous fungi of the order, Mucorales of the Mucoraceae family.
• Rhino-Orbital Mucormycosis (ROM) is a rare disease with an overall
prevalence of 0.15% of the diabetic.
• Despite the advances in the diagnosis and treatment, a high mortality
rate of 30-70% still exists for this disease.
• It is an aggressive fungal infection which is seen in
immunocompromised hosts.

19. • The risk factors are poorly controlled Diabetes mellitus,
haematological malignancies and a prolonged corticosteroid
treatment.
• Death may occur within two weeks in untreated or unsuccessfully
cases.
• The infections which are caused by members of the order mucorales
are primarily opportunistic infections .
 They represent the third leading cause of invasive fungal infections
following Aspergillus and Candida species.

20. Presentation- is with gradual onset facial and periorbital swelling,
diplopia and visual loss.
Signs-ischaemic infarction superimposed on septic necrosis is responsible
for black eschar which develops on palate, turbinates, nasal septum, skin
and eyelids.

21.  Pathogenesis- infection is acquired by inhalation of spores giving
rise to upper respiratory infection which spreads to the sinuses and
subsequently to the orbit and brain.
 Invasion of blood vessels by hyphae results in occlusive vasculitis
with ischaemic infarction of orbital tissue.
 Complication- retinal vascular occlusion
multiple cranial nerve palsies

22. Treatment
 Intravenous antifungal agents such as amphotericin.
 Daily packing and irrigation of involved area with amphotericin.
 Wide excision of devitalised and necrotic tissue.
 Correction of underlying metabolic defect
 Exenteration required in unresponsive cases.

23. Idiopathic Orbital Inflammatory Disease (IOID)
• It is a disorder characterised by non-neoplastic,non infective, space
occupying orbital lesion.
• Histopathalogy reveals pleomorphic inflammatory infiltrates
• It was previously known as orbital pseudotumour
• The inflammatory process may involve any or all orbital tissue
resulting in myositis,dacryoadenitis or scleritis.
• Paranasal sinuses are usually clear.

24. Sign
• Usually unilateral
• Periorbital swelling and chemosis
• Proptosis
• Ophthalmoplegia

25. course
 Spontaneous remission after a few weeks without sequelae.
 Severe prolonged inflammation eventually leading to progressive
fibrosis of orbital tissues, resulting in a frozen orbit .
 Associated with ptosis and visual impairement caused by optic nerve
involvement.

26. Investigations-
 Brief history
 Complete ocular examination
 Orbital CT ( axial and coronal)
 Blood investigations
 Biopsy is generally required in persistent cases to confirm the
diagnosis.
Treatment-
 Systemic steroid- administered only after the diagnosis has been
confirmed . Initially 60-80 mg/day and later tapered.
 Radiotherapy if no improvement after 2 weeks of adequate steroid
therapy. Even low dose (10 Gy) produces remission.

27.  Antimetabolites- such as methotrexate or mycophenolate mofetil
may be necessary if there is resistance to steroid and radiotherapy.
 Systemic infliximab effective in recurrent cases

28. Tolosa -Hunt syndrome
• Rare idiopathic condition caused by non-specific granulomatous
inflammation of the -
• cavernous sinus
• superior orbital fissure
• orbital apex
• It is a diagnosis of exclusion.
• Prevalence – estimated annual incidence is one case per million per
year.
• Males and females are equally affected.

29. Etiology - remains unknown.
• no information is available as to what triggers the inflammatory process
in the region of the cavernous sinus/superior orbital fissure.
• thus syndrome falls within the range of idiopathic orbital inflammation
(pseudotumour)
Sign-
• Proptosis
• Ocular motor nerve palsies often with involvement of the pupil.
• Sensory loss along the distribution of the first and second divisions of
the trigeminal nerve.
• Gnawing pain may precede ophthalmoplegia

30.  The International headache society include following criteria for
Tolosa-Hunt syndrome -
 Episode(s) of unilateral orbital pain for an average of 8 weeks if left
untreated
 Associated paresis of the third, forth, or sixth cranial nerves, which
may coincide with onset of pain or follow it by a period of up to 2
weeks
 Pain that is relieved within 72 hours of steroid therapy initiation
 Exclusion of other conditions by neuroimaging and angiography

31. Investigations –
 CBC count
 erythrocyte sedimentation rate (ESR)
 electrolytes with glucose,
 thyroid function tests,
 fluorescent treponemal antibody (FTA)
 antinuclear antibody (ANA),
 antineutrophil cytoplasmic antibody (ANCA)
 fungal and/or bacterial cultures, Gram stain.
 CSF

32.  Corticosteroids are the treatment of choice.
 usually providing significant pain relief within 24-72 hours of
therapy initiation.
 Ophthalmoparesis usually requires weeks to months for resolution;
indeed, ophthalmoparesis may not completely resolve in some cases
depending on the degree of inflammation and the aggressiveness of
therapy.
 For refractory cases, azathioprine (Imuran), methotrexate, or
radiation therapy has been employed

33. Orbital myositis
• It is an idiopathic , non specific inflammation of one or more
extraocular muscles .
• Considered a subtype of IOID.
• Presentation – most commonly affects young adults in the third
decade of life, with a female predilection.
• Histology – chronic inflammatory cellular infiltrate
• Signs –
• Lid oedema,ptosis and chemosis
• Vascular congestion over involved muscles.
• Chronic cases- affected muscles may become fibrosed, with
permanent restrictive myopathy.

34.  Course – acute non-recurrent involvement which resolves
spontaneously within 6 weeks.
 Chronic disease characterized by either a single episode persisting
for longer than 2 months or recurrent attacks.
 Treatment –
 NSAIDs adequate in mild disease
 Systemic steroids are generally required and produce dramatic
improvement.
 Radiotherapy- effective,if above treatment fails.

35. Vascular congestion over involved
muscle
Ct- scan- enlargement of muscle

36. Dacryoadenitis
• Lacrimal gland involvement occurs in 25% of patients
with IOID.
• More commonly occurs in isolation, resolves spontaneously
without treatment.
• Etiology –
• most common- inflammatory non- infectious.
• rare- bacterial, usually due to S. aureus , N. gonorrhoeae.
• Viral- mumps, influenza, infectious mononucleosis.
• Typically occurs in children and young adults.

37. Signs-
• Swelling of the lateral aspect of the eyelid giving rise to a
characteristic s-shaped ptosis and slight downward and inward
displacement.
• Tenderness over the lacrimal gland fossa.
• Injection of the palpebral portion of the lacrimal gland and adjacent
conjunctiva.
Treatment- if specific etiology is unclear treat the patient empirically
with systemic antibiotics.
• Clinical response to antibiotic can guide further management and in
unresponsive cases steroid therapy can be started.

38. • Oedema of lateral aspect of upper lid
• Mild downward and inward globe
displacement
Injection and tenderness of
lacrimal gland

39. Thyroid related orbitopathy
 TED or Graves ophthalmopathy
 Auto-immune
 IgG antibodies bind to thyroid TSH receptors in the thyroid gland
and stimulate secretion of thyroid hormone.
 80% of patients with TRO are hyperthyroid
 10% are hypothyroid
 10% are euthyroid

40.  Sex predilection F:M- 3:1
 Smokers with TRO have more severe disease.
 Common in 3rd-4th decade of life
 Familial tendency with family history of thyroid disease in
approximately 30% of cases.
Association with systemic disease-
 Pernicious anaemia
 Addison's disease
 Rheumatoid arthritis
 Diabetes mellitus
 Idiopathic thrombocytopenic purpura
 Myasthenia gravis

41. Pathogenesis-
 Autoimmune Disorder (IgG mediated)
 Enlargement of Extraocular Muscles
-by increase in glycosaminoglycans (GAG)
 Cellular Infiltration of Interstitial Tissues
-with lymphocytes, plasma cells, macrophages & mast cells
-Fibrosis
 Proliferation of Orbital Fat, Connective Tissue and Lacrimal Gland
-with retention of fluid & accumulation of GAG
41

42.  Characterized by inflammation and enlargement of orbital
tissues, extra ocular muscles sparing tendon
 Gross examination -extra ocular muscles are enlarged, firm,
rubbery, and dark red
42

43. 43
Stages of TED
Acute, active, inflammatory ( congestive) stage-
• Eyes are red and painful
• Tends to remit within 3 years
• Only 10% patient develop serious long term
complication.

44. Chronic, stable ( Fibrotic) stage-
• Hypertrophy and fibrosis of extra ocular muscles
• painless motility defect
• White eyes
44

45. 45
Congestive phase
Fibrotic phase

46. Signs:
 Lid retraction
 Lid lag
 Restrictive EOM movement
 Proptosis
 ON compression

47. Proptosis
 Axial
 Uni/bilateral
 Inflammatory cells infiltration  GAG  fluid retention 
increase orbital pressure  proptosis

48. Lid retraction
Occurs in 50% of patient with Graves disease.
Dalrymple sign- lid retraction in primary gaze
Kocher sign- staring or frightened appearance of eye
Von graefe sign- retarded descent of upperlid on downgaze.
kocher sign
Von Graefe Sign

49. Restrictive myopathy –
• occurs in 30%-50% of patients with TED.
• Ocular motility restricted initially by inflammatory oedema and later
by fibrosis.
• Inferior rectus muscle most commonly involved.
Optic neuropathy-
• Uncommon but serious complication caused by compression of
optic nerve at orbital apex by congested and enlarged recti.
• Visual acuity is reduced, RAPD, colour vision impairement and
diminshed light brightness impairement.
• optic disc is usually normal

50. Treatment
 Supportive care
 Systemic corticosteroids
 Orbital radiation treatment
Surgery-
 orbital decompression
 Strabismus surgery-
 Eyelid surgery

51. Oral steroid-
indications- congestive phase ( pain/rapid progressive)
start with 60-80mg/day
Reduction of S/S usually occurs within 48 hours
Maximal response 2-8 weeks
Discontinue after about 3 months though long term maintenance may
be necessary
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52.  Intravenous Methyl prednisolone
• Indication -usually reserved for compressive neuropathy
dose- 0.5 -1 gm /d for 3-5 days.
 Radiotherapy
• Indication- steroid ineffective or contraindicated cases
• Positive response is usually seen in 6 weeks and maximal
improvement in 4 months
• A cobalt-60 unit delivers total dose of 2000 cGy radiation in 10
fractions over 2 wk.
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53. Surgical Decompression
Indications :- Compressive optic neuropathy
Exposure keratopathy ( Severe)
Cosmetic
Goals :- of orbital decompression-
Expanding orbital volume (bony expansion)
Reducing orbital soft tissue(fat decompression)

54.  One wall decompression (lateral wall)
4-5 mm reduction in proptosis
 Two wall (balanced medial and lateral wall)
5-6 mm reduction in ptosis
 Three wall decompression includes floor
reduction in proptosis of 6-10 mm.
 four wall decompression
Very severe proptosis – may require additional removal of orbital
roof
 Complication of orbital decompression –
 Risk of visual loss
 Bleeding and infection

55. Thank you