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Case presentation
Presenter : Dr Rukkaiya Khan (2nd year resident )
Moderator : Dr Urmila Mam
DHIR HOSPITAL AND POST GRADUATE INSTITUTE OF
OPHTHALMOLOGY
PATIENT DETAILS
 35 year old male
 Taxi driver
 Bhiwani , Haryana presented in OPD in July 2023
CHIEF COMPLAINT
 Swelling in LE since 1 month
 Double vision in LE since 10 days
HOPI
 Patient was apparently asymptomatic untill 2 months back when he noticed mild
swelling in LE associated with pain and redness which was progressive in nature
and worse in morning
 He visited local ophthalmologist and received t/t on the lines of localized
episcleritis , improved symptomatically
 Later on he developed c/o double vision in LE since 10 days which was acute in
onset associated with pain which is non radiating present both at rest and with
movements
 No h/o defective vision or blackouts or transient loss of vision or defective colour
perception
 No h/o postural variation
HISTORY
 Past History :
– No h/o trauma , malignancy ,systemic disease
– No h/o diabetes , hypertension or cardiac disease
– No h/o weight loss ,sweating ,tremors ,palpitations, hyperpigmentation of lid /eyes or skin
discoloration
– No h/o radiation therapy or chemotherapy
– No h/o steroid intake
– No h/o dysphagia ,dysphonia ,easy fatigability ,drooping of eyelids
– No history of fever /headache /nausea /vomiting chronic cough
 Personal history :
– Mixed diet / normal bowel and bladder habit
– Chronic smoker consumes average 4-5 cigarettes per day
– Occasionally consumes alcohol
 Family history : No history of diabetes /HTN /cardiac ds or similar symptoms
among family members
 Past ocular history :
– Wear glasses
– No history of any intraocular surgery
 Surgical History : no h/o any previous surgery
GENERAL EXAMINATION
 Patient is conscious ,oriented to time place person
 Patient average built and nourished
 Pulse : 84 bpm
 RR: 14/ min
 BP : 130/88
 No pallor ,icterus , cyanosis , clubbing , lymphadenopathy , pedal edema
ON TORCH LIGHT EXAMINATION
 Inspection
– Lid : both UL and LL swelling , periocular swelling
– Lagopthalmos in LE
 On palpation
– LE : feel warm then the surrounding skin
– No mass felt
– Retropulsion test +ve
– Finger insinuation : palpating between orbit and glove
– Sensations : intact
 Auscultation
– No bruits heard in LE
ON TORCH LIGHT EXAMINATION
 Hertel’s exopthalomometry (base 104 )
– RE - 12 mm
– LE - 15 mm
OPHTHALMIC WORKUP
Visual acuity RE LE
Unaided 6/6p 6/6p
Aided 6/6 6/6
Sub ref -0.50 *45 with
+1.00 N 06
-0.50 with
+1.00 N 06
Colour vision Normal Normal
External examination
Facial symmetry Symmetrical on both sides
External face Normal
Head posture Normal
Ocular position Orthotropic in OU
Ocular movements Full ,free and painless in RE.
Supero-lateral and inferior
movement restriction in LE
1st visit
SLIT LAMP EXAMINATION RE LE
Eyelids Flat UL and LL swelling
Periocular swelling
Conjunctiva Normal Nasal Congestion
Cornea Clear
Stain –ve
Clear
Stain –ve
Anterior chamber Normal in content and depth ,
VH –IV
Normal in content and depth ,
VH –IV
Iris Normal colour and pattern Normal colour and pattern
Pupil Round ,reacting , no RAPD Round ,reacting , no RAPD
Lens Clear Clear
IOP on AT 16 mm of HG 15 mm of HG
SLIT LAMP EXAMINATION
FUNDUS EXAMINATION
FUNDUS
EXAMINATION
RE LE
PVD Absent Absent
Optic disc Medium size, vertically
oval
Medium size, vertically oval
with blurred margins
C/D Ratio 0.2 Edematous
Macula Centrally appears to be
normal
Choroidal folds
Fundus No t/t lesion seen No t/t lesion in periphery
DIFFERENTIAL DIAGNOSIS
 Thyroid ophthalmopathy
 Oribital pseudotumor
 Orbital cellulitis
 Orbital tumors
 Inflammatory orbitopathy –granulomatous with polyangitis
PROVISIONAL DIAGNOSIS
 Orbital cellulitis
 TED
 Oribital pseudotumor
INVESTIGATIONS
 OCT /FP
 CBC with ESR
 RBS
 Thyroid profile
 CECT brain + Orbit
 Hb : 13 gm/dl
 RBC : 3.25
 TLC : 7.2
 Random BS : 112 mg/dl
 S. urea : 32.2 mg/dl
 S.Creatinine : 0.98 mg/dl
 Thyroid profile : NA
 Contrast enhanced CT orbit : shows mild fat stranding in retrobulbur
region –S/O Mild retrobulbur cellulitis changes
 NCCT head : Normal
Treatment :
 Oral prednisolone 60mg /day given for 1 weeks
 Tab pantoprazole 40mg / day
 E/D moxifloxacin 0.5 %+ loteprednol 0.5 % QID for 1 week
On f/u after 1 week :
LE :
 OM improved except for
inferior gaze
 Conjunctival congestion
improved
 Disc edema reduced / FR +
 Hertel’s ( base 104 ) :
RE 12 LE 15
 DIAGNOSIS : LE Orbital Pseudotumor
TREATMENT
 E/D moxifloxacin + loteprednol E/D ( QID ) and oral steroids 60 mg /day
gradually tapered over 4 weeks
 At 1 month f/u ocular movements improved except for diplopia in down
gaze , on hertels with 104 base RE 12 LE 12
 Kept on maintenance dose of oral steroid 10 mg /day
Last visit
NON SPECIFIC ORBITAL INFLAMMATORY
DISEASE (NSOIDS)
 Non specific ,benign ,idiopathic ,inflammatory process ,characterized by
polymorphous lymphoid infiltrates and varying degree of fibrosis without any
identifiable local or systemic causes
 Was first described by Gleason in 1903
 Can be acute ,subacute and chronic
 Tissue eosinophilia
 Granulomatous inflammation
 Vasculitis
 Marked desmoplasia
 Diagnosis of exclusion
SYMPTOMS
 Immune mediated pathology –associated with Chron’s ,SLE ,RA Ankyosing
spondyitis , Myasthenia , Diabetes
 Acute or recurrent, orbital pain and prominent red eyes
 Pink eyelid edema
 DOV , Double vision
 Children : Constitutional symptoms (fever ,headache ,vomiting ,
abdominal pain and lethargy )
SIGNS
 Proptosis and restricted eye movement usually unilateral
 Soft tissue involvement of varying degree
 Conjunctival congestion and chemosis
 Eyelid erythema and swelling
 Impaired vision and hyperopic shift
 Decreased corneal sensitivity
 Elevated IOP
 Uveitis, optic nerve swelling and atrophy
Rootman and Nugent classified acute orbital
pseudotumors according to their orbital
location, and described five patterns:
 Lacrimal
 Myositic
 Diffuse
 Anterior
 Apical
OID SITES
 Dacryoadenitis of Lacrimal glands
 Myositis of extraocular muscles
 Perineuritis of optic nerve
 Orbital cellulitis
 Orbital apicitis ( Tolosa Hunt Syndrome
 Periscleritis
 Diffuse orbital inflammatory disease
DACRYOADENITIS
 Inflammation and diffuse enlargement of the
lacrimal gland including palpebral and orbital
lobes
 Painful, firm, erythematous mass with edema
in lateral UL , and possible ptosis
 “almond-shaped” appearance of the gland
with a tapered posterior margin of the gland
 With inflammation of the surrounding soft
tissue
D/D
 Epithelial neoplasm
– Typically involves only a portion of the lacrimal gland, usually the orbital lobe
– Well-circumscribed and round to oval in shape
 Orbital lymphoma
– Diffuse lacrimal gland enlargement without infiltration of surrounding fat
– to distinguish lymphoma from inflammatory disease – DWI
– The densely packed cells in lymphoma inhibit the non- random motion of water, causing
lymphoma to appear bright on DWI
MYOSITIS
 Non-infectious inflammation of extraocular
muscles
 Clinically presents as
– Unilateral orbital or periorbital pain
– Painful and restricted eye movement
– Proptosis
– Periorbital edema
– Hyperemia of the conjunctiva
 Classic appearance- unilateral thickening of one
or two EOMs, also involving the surrounding
fat, tendon, and myotendinous junction
Bilateral MR and LR tubular-like
enlargement with tendon involvement
D/D
 Thyroid disease
– Differentiation from thyroid disease -- Unilateral disease, infiltration of the surrounding fat,
and early involvement of the superior oblique muscle
 IgG4 related disease
 Orbital cellulitis
– fever ,leucocytosis ,clinical h/o head and neck infection
 Metastasis and lymphoma –focal mass with increased signal density in EOM
 Low flow Carotid cavernous fistula (CCF )
– Transcranial doppler ultrasonography allows visualization of retrograde flow through the
Superior ophthalmic vein s/o CCF
IgG4-RD
• Multiorgan mass lesion
• Infiltration of plasma cells ,T-cells
• Elevated acute phase reactants ,serum IgG4
• Associated with dacryoadenitis ,xanthogranuloma ,orbital amyloidosis
• Respond well with steroids
DIFFUSE CELLULITIC ORBITAL
INFLAMMATION
 Inflammation of preseptal (peri-orbital) or postsetpal (orbital) fat
 Present with proptosis, chemosis, and painful diplopia , vision reduction
associated perineuritis
 Unilateral and Repeated episodes
 Best evaluated on contrast-enhanced T1 MRI with fat suppression -- poorly-
defined periorbital enhancement enveloping the globe and extending into
post-septal fat
 Infectious cellulitis -clinical history of fever, sinusitis, or meningitis
,leukocytosis, presence of an abscess
 On T2 MRI, infectious cellulitis typically presents as a hyperintense lesion,
whereas OID lesions range from to hypo- to hyperintense.
D/D
 Infection, CCF, cavernous sinus thrombosis, and Wegener’s granulomatosis
 CCF
– enlarged SOV, abnormal fullness of the cavernous sinus, or, in larger fistulas, flow voids on
T2 MRI
 Cavernous sinus thrombosis
– Enlarged SOV
– Non-enhancing filling defect in the cavernous sinus on CT venography or contrast-
enhanced MRI differentiates cavernous sinus thrombosis from CCF or OID
 Wegener’s granulomatosis (granulomatosis with polyangiitis)
– often accompanied by surrounding sinonasal wall destruction(CT )
CELLULITIS
OPTIC PERINEURITIS
 Intraorbital inflammation extending along optic nerve and nerve sheath
but affecting the nerve sheath rather than the nerve
 Primary presenting clinical feature is pain, while visual acuity, visual fields,
and color vision are typically unaffected
 On post-gadolinium T1 MRI with fat suppression- increased signal intensity
surrounding the optic nerve
 MRI of perineuritis - “tram-track” pattern of enhancement around the
nerve
D/D
 Optic nerve sheath meningioma
– Localized mass and calcifications on CT imaging
 Demyelinating optic neuritis
– Almost always spares the soft tissues around the nerve while involving the nerve
substance diffusely
CT image of optic nerve involvement with sheath enhancement ("tramline" sign),
white arrow showing right lacrimal gland enlargement
 Axial fat suppressed
contrast enhanced T1
weighted : well defined
enhancement of localized
mass in optic nerve sheath
 Meningioma of right optic
nerve sheath
PERISCERITIS
 Inflammation of the sclera, uvea (iris, ciliary body, choroid), or tenon’s
capsule
 Clinically characterized by orbital pain, exophthalmos, and eyelid edema
 Periscleritis can be clearly seen on MR or CT as a heterogeneous
thickening along the outer rim of the eye.
 Axial T1 post-contrast MRI with fat saturation -- visualization of the
enhancing vascular choroid as well as any extension into retrobulbar fat
 A subchoroidal fluid collection displacing the retina.
D/D
 Systemic inflammatory disease that causes posterior scleritis, such as
lupus or rheumatoid arthritis
 Infectious periscleritis often arises secondary to sinus infection particularly
the ethmoid sinus, in patients with uveoscleral thickening
CT image showing
thickening and blurring of
left eye uveoscleral
FOCAL INFLAMMATORY MASS
 M/C/C of painful orbital mass in adults
 Mass lesion in OID best seen on axial T2 MRI -- appears as a well-defined,
T2 hypointense mass
 On T1 MRI -- slightly brighter, isointense to muscle, and show prominent
postgadolinium enhancement
 OID may present with eyelid edema, optic nerve atrophy, and conjunctival
congestion, marked T2 hypointensity and evidence of fibrosis.
D/D
 Lymphoma typically appears more lobular and has greater diffusion
restriction than OID on DWI
 Metastases are usually brighter on T2 imaging
 One exception -- scirrhous breast cancer metastasis, which commonly
produces a T2-hypointense, fibrotic mass with variable amount of traction
on adjacent structures
 Benign tumors, such as solitary fibrous tumor, can also show marked T2
hypointensity and overlap with OID in appearance
DIFFUSE OID
 Seen in 11 % of patients
 Patients must be evaluated for systemic disease, including vasculitis and
autoimmune conditions such as Churg-Strauss disease or Wegener’s
granulomatosis
 Common characteristics of orbital involvement in Wegener’s include diffuse
infiltration of orbital fat and sinonasal destructive changes
 Chest imaging and an immunologic workup are suggested prior to biopsy of
diffuse OID
 Lymphoma may also mimic diffuse OID and appears more lobular and best
distinguished from OID using DWI MRI
 Chronic inflammation often contains regions with varying degrees of fibrosis --
heterogeneous appearance on MRI
ORBITAL APICITIS
 Involvement of the orbital
apex
 Less common
 Associated with the poorest
outcome
 Inflammatory lesions of the
orbital apex are at risk of
invading the optic nerve or
extending into the cavernous
sinus
MRI, fat-saturated, T1-weighted image with white
arrows showing extension into the cavernous sinus
 Tolosa-Hunt syndrome is a rare clinical condition caused by cavernous sinus
inflammation presenting with relapsing/remitting acute orbital pain and
paralysis of cranial nerves Ⅲ, Ⅳ, Ⅴ1, and Ⅵ
 Extension of OID into the cavernous sinus is a common cause of this clinical
condition
 On T1 MRI, inflammation appears as an intermediate intensity lesion, as
inflammatory tissue replaces the normal high-intensity fat at the orbital
apex
 OID of the orbital apex appears hypointense on T2, with a darker signal
indicating higher degrees of fibrosis.
D/D
 Meningioma, granulomatous disease, and local spread of central nervous
system (CNS) pathology
 Common features of CNS involvement include abnormal soft tissue
extending into the middle cranial fossa, expansion of the ipsilateral
cavernous sinus walls, and post-gadolinium enhancement of the meninges
or dura
INVESTIGATIONS
 CBC with ESR
 ANA
 S.ACE
 C-ANCA and p-ANCA
 BUN/creatinine
 FBS /HBA1C
Biopsy may be considered if there are
progressive neurologic deficits, lack of steroid
responsiveness and persistent imaging
abnormalities.
Imaging -CT and MRI findings
• Orbital CT with contrast : may show thickened posterior sclera ,orbital fat ,
lacrymal gland involvement or thickening of EOM
• Orbital MRI with contrast and fat suppressed : may show EOM
enlargement ,orbital fat infiltration ,lacrymal gland enlargement ,
thickening of posterior tenon / sclera and enhancement along the optic
nerve
Differential Diagnosis
 Thyroid related orbitopathy
 Orbital cellulitis +/- Abscess
 Non infectious OID : sarcoidosis , IgG 4 reated orbitopathy ,amyoidosis
,eosinophelia ,,GPA ,RA,SLE ,Sjogrens syndrome
 Lymph proliferative diseases
 Primary orbital malignancy
 Metastasis
 Vascular malformations : CCF
 Cavernous hemangioma
Treatment
 Observation
 NSAIDS
 High dose steroid – Acute/Subacute OID. Prednisoone -1 mg /kg/day
Tapering should be done over months
 Low dose Radiotherapy
 Methotrexate ( 15 – 20 mg ),cyclophosphamide -steroid sparing agent
 MMF ,Azathioprine ,
 Calcineurin nhibitors : cyclosporine, tacrolimus
 Refractory cases – Anti TNF – alpha inhibitors
 Biologic therapy -I.V infliximab, S.C Adalimumab and Etanercept
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orbital_pseudotumor presentation dhir hospital bhiwani.pptx

  • 1. Case presentation Presenter : Dr Rukkaiya Khan (2nd year resident ) Moderator : Dr Urmila Mam DHIR HOSPITAL AND POST GRADUATE INSTITUTE OF OPHTHALMOLOGY
  • 2. PATIENT DETAILS  35 year old male  Taxi driver  Bhiwani , Haryana presented in OPD in July 2023
  • 3. CHIEF COMPLAINT  Swelling in LE since 1 month  Double vision in LE since 10 days
  • 4. HOPI  Patient was apparently asymptomatic untill 2 months back when he noticed mild swelling in LE associated with pain and redness which was progressive in nature and worse in morning  He visited local ophthalmologist and received t/t on the lines of localized episcleritis , improved symptomatically  Later on he developed c/o double vision in LE since 10 days which was acute in onset associated with pain which is non radiating present both at rest and with movements  No h/o defective vision or blackouts or transient loss of vision or defective colour perception  No h/o postural variation
  • 5. HISTORY  Past History : – No h/o trauma , malignancy ,systemic disease – No h/o diabetes , hypertension or cardiac disease – No h/o weight loss ,sweating ,tremors ,palpitations, hyperpigmentation of lid /eyes or skin discoloration – No h/o radiation therapy or chemotherapy – No h/o steroid intake – No h/o dysphagia ,dysphonia ,easy fatigability ,drooping of eyelids – No history of fever /headache /nausea /vomiting chronic cough  Personal history : – Mixed diet / normal bowel and bladder habit – Chronic smoker consumes average 4-5 cigarettes per day – Occasionally consumes alcohol
  • 6.  Family history : No history of diabetes /HTN /cardiac ds or similar symptoms among family members  Past ocular history : – Wear glasses – No history of any intraocular surgery  Surgical History : no h/o any previous surgery
  • 7. GENERAL EXAMINATION  Patient is conscious ,oriented to time place person  Patient average built and nourished  Pulse : 84 bpm  RR: 14/ min  BP : 130/88  No pallor ,icterus , cyanosis , clubbing , lymphadenopathy , pedal edema
  • 8. ON TORCH LIGHT EXAMINATION  Inspection – Lid : both UL and LL swelling , periocular swelling – Lagopthalmos in LE  On palpation – LE : feel warm then the surrounding skin – No mass felt – Retropulsion test +ve – Finger insinuation : palpating between orbit and glove – Sensations : intact  Auscultation – No bruits heard in LE
  • 9. ON TORCH LIGHT EXAMINATION  Hertel’s exopthalomometry (base 104 ) – RE - 12 mm – LE - 15 mm
  • 10. OPHTHALMIC WORKUP Visual acuity RE LE Unaided 6/6p 6/6p Aided 6/6 6/6 Sub ref -0.50 *45 with +1.00 N 06 -0.50 with +1.00 N 06 Colour vision Normal Normal External examination Facial symmetry Symmetrical on both sides External face Normal Head posture Normal Ocular position Orthotropic in OU Ocular movements Full ,free and painless in RE. Supero-lateral and inferior movement restriction in LE
  • 12. SLIT LAMP EXAMINATION RE LE Eyelids Flat UL and LL swelling Periocular swelling Conjunctiva Normal Nasal Congestion Cornea Clear Stain –ve Clear Stain –ve Anterior chamber Normal in content and depth , VH –IV Normal in content and depth , VH –IV Iris Normal colour and pattern Normal colour and pattern Pupil Round ,reacting , no RAPD Round ,reacting , no RAPD Lens Clear Clear IOP on AT 16 mm of HG 15 mm of HG SLIT LAMP EXAMINATION
  • 13. FUNDUS EXAMINATION FUNDUS EXAMINATION RE LE PVD Absent Absent Optic disc Medium size, vertically oval Medium size, vertically oval with blurred margins C/D Ratio 0.2 Edematous Macula Centrally appears to be normal Choroidal folds Fundus No t/t lesion seen No t/t lesion in periphery
  • 14. DIFFERENTIAL DIAGNOSIS  Thyroid ophthalmopathy  Oribital pseudotumor  Orbital cellulitis  Orbital tumors  Inflammatory orbitopathy –granulomatous with polyangitis
  • 15. PROVISIONAL DIAGNOSIS  Orbital cellulitis  TED  Oribital pseudotumor
  • 16. INVESTIGATIONS  OCT /FP  CBC with ESR  RBS  Thyroid profile  CECT brain + Orbit
  • 17.  Hb : 13 gm/dl  RBC : 3.25  TLC : 7.2  Random BS : 112 mg/dl  S. urea : 32.2 mg/dl  S.Creatinine : 0.98 mg/dl  Thyroid profile : NA
  • 18.  Contrast enhanced CT orbit : shows mild fat stranding in retrobulbur region –S/O Mild retrobulbur cellulitis changes  NCCT head : Normal
  • 19. Treatment :  Oral prednisolone 60mg /day given for 1 weeks  Tab pantoprazole 40mg / day  E/D moxifloxacin 0.5 %+ loteprednol 0.5 % QID for 1 week
  • 20. On f/u after 1 week : LE :  OM improved except for inferior gaze  Conjunctival congestion improved  Disc edema reduced / FR +  Hertel’s ( base 104 ) : RE 12 LE 15
  • 21.  DIAGNOSIS : LE Orbital Pseudotumor
  • 22. TREATMENT  E/D moxifloxacin + loteprednol E/D ( QID ) and oral steroids 60 mg /day gradually tapered over 4 weeks  At 1 month f/u ocular movements improved except for diplopia in down gaze , on hertels with 104 base RE 12 LE 12  Kept on maintenance dose of oral steroid 10 mg /day
  • 24. NON SPECIFIC ORBITAL INFLAMMATORY DISEASE (NSOIDS)  Non specific ,benign ,idiopathic ,inflammatory process ,characterized by polymorphous lymphoid infiltrates and varying degree of fibrosis without any identifiable local or systemic causes  Was first described by Gleason in 1903  Can be acute ,subacute and chronic  Tissue eosinophilia  Granulomatous inflammation  Vasculitis  Marked desmoplasia  Diagnosis of exclusion
  • 25. SYMPTOMS  Immune mediated pathology –associated with Chron’s ,SLE ,RA Ankyosing spondyitis , Myasthenia , Diabetes  Acute or recurrent, orbital pain and prominent red eyes  Pink eyelid edema  DOV , Double vision  Children : Constitutional symptoms (fever ,headache ,vomiting , abdominal pain and lethargy )
  • 26. SIGNS  Proptosis and restricted eye movement usually unilateral  Soft tissue involvement of varying degree  Conjunctival congestion and chemosis  Eyelid erythema and swelling  Impaired vision and hyperopic shift  Decreased corneal sensitivity  Elevated IOP  Uveitis, optic nerve swelling and atrophy
  • 27. Rootman and Nugent classified acute orbital pseudotumors according to their orbital location, and described five patterns:  Lacrimal  Myositic  Diffuse  Anterior  Apical
  • 28. OID SITES  Dacryoadenitis of Lacrimal glands  Myositis of extraocular muscles  Perineuritis of optic nerve  Orbital cellulitis  Orbital apicitis ( Tolosa Hunt Syndrome  Periscleritis  Diffuse orbital inflammatory disease
  • 29.
  • 30. DACRYOADENITIS  Inflammation and diffuse enlargement of the lacrimal gland including palpebral and orbital lobes  Painful, firm, erythematous mass with edema in lateral UL , and possible ptosis  “almond-shaped” appearance of the gland with a tapered posterior margin of the gland  With inflammation of the surrounding soft tissue
  • 31. D/D  Epithelial neoplasm – Typically involves only a portion of the lacrimal gland, usually the orbital lobe – Well-circumscribed and round to oval in shape  Orbital lymphoma – Diffuse lacrimal gland enlargement without infiltration of surrounding fat – to distinguish lymphoma from inflammatory disease – DWI – The densely packed cells in lymphoma inhibit the non- random motion of water, causing lymphoma to appear bright on DWI
  • 32.
  • 33.
  • 34. MYOSITIS  Non-infectious inflammation of extraocular muscles  Clinically presents as – Unilateral orbital or periorbital pain – Painful and restricted eye movement – Proptosis – Periorbital edema – Hyperemia of the conjunctiva  Classic appearance- unilateral thickening of one or two EOMs, also involving the surrounding fat, tendon, and myotendinous junction Bilateral MR and LR tubular-like enlargement with tendon involvement
  • 35. D/D  Thyroid disease – Differentiation from thyroid disease -- Unilateral disease, infiltration of the surrounding fat, and early involvement of the superior oblique muscle  IgG4 related disease  Orbital cellulitis – fever ,leucocytosis ,clinical h/o head and neck infection  Metastasis and lymphoma –focal mass with increased signal density in EOM  Low flow Carotid cavernous fistula (CCF ) – Transcranial doppler ultrasonography allows visualization of retrograde flow through the Superior ophthalmic vein s/o CCF
  • 36.
  • 37.
  • 38. IgG4-RD • Multiorgan mass lesion • Infiltration of plasma cells ,T-cells • Elevated acute phase reactants ,serum IgG4 • Associated with dacryoadenitis ,xanthogranuloma ,orbital amyloidosis • Respond well with steroids
  • 39. DIFFUSE CELLULITIC ORBITAL INFLAMMATION  Inflammation of preseptal (peri-orbital) or postsetpal (orbital) fat  Present with proptosis, chemosis, and painful diplopia , vision reduction associated perineuritis  Unilateral and Repeated episodes  Best evaluated on contrast-enhanced T1 MRI with fat suppression -- poorly- defined periorbital enhancement enveloping the globe and extending into post-septal fat  Infectious cellulitis -clinical history of fever, sinusitis, or meningitis ,leukocytosis, presence of an abscess  On T2 MRI, infectious cellulitis typically presents as a hyperintense lesion, whereas OID lesions range from to hypo- to hyperintense.
  • 40. D/D  Infection, CCF, cavernous sinus thrombosis, and Wegener’s granulomatosis  CCF – enlarged SOV, abnormal fullness of the cavernous sinus, or, in larger fistulas, flow voids on T2 MRI  Cavernous sinus thrombosis – Enlarged SOV – Non-enhancing filling defect in the cavernous sinus on CT venography or contrast- enhanced MRI differentiates cavernous sinus thrombosis from CCF or OID  Wegener’s granulomatosis (granulomatosis with polyangiitis) – often accompanied by surrounding sinonasal wall destruction(CT )
  • 42.
  • 43. OPTIC PERINEURITIS  Intraorbital inflammation extending along optic nerve and nerve sheath but affecting the nerve sheath rather than the nerve  Primary presenting clinical feature is pain, while visual acuity, visual fields, and color vision are typically unaffected  On post-gadolinium T1 MRI with fat suppression- increased signal intensity surrounding the optic nerve  MRI of perineuritis - “tram-track” pattern of enhancement around the nerve
  • 44. D/D  Optic nerve sheath meningioma – Localized mass and calcifications on CT imaging  Demyelinating optic neuritis – Almost always spares the soft tissues around the nerve while involving the nerve substance diffusely
  • 45. CT image of optic nerve involvement with sheath enhancement ("tramline" sign), white arrow showing right lacrimal gland enlargement
  • 46.
  • 47.  Axial fat suppressed contrast enhanced T1 weighted : well defined enhancement of localized mass in optic nerve sheath  Meningioma of right optic nerve sheath
  • 48. PERISCERITIS  Inflammation of the sclera, uvea (iris, ciliary body, choroid), or tenon’s capsule  Clinically characterized by orbital pain, exophthalmos, and eyelid edema  Periscleritis can be clearly seen on MR or CT as a heterogeneous thickening along the outer rim of the eye.  Axial T1 post-contrast MRI with fat saturation -- visualization of the enhancing vascular choroid as well as any extension into retrobulbar fat  A subchoroidal fluid collection displacing the retina.
  • 49.
  • 50. D/D  Systemic inflammatory disease that causes posterior scleritis, such as lupus or rheumatoid arthritis  Infectious periscleritis often arises secondary to sinus infection particularly the ethmoid sinus, in patients with uveoscleral thickening
  • 51. CT image showing thickening and blurring of left eye uveoscleral
  • 52. FOCAL INFLAMMATORY MASS  M/C/C of painful orbital mass in adults  Mass lesion in OID best seen on axial T2 MRI -- appears as a well-defined, T2 hypointense mass  On T1 MRI -- slightly brighter, isointense to muscle, and show prominent postgadolinium enhancement  OID may present with eyelid edema, optic nerve atrophy, and conjunctival congestion, marked T2 hypointensity and evidence of fibrosis.
  • 53. D/D  Lymphoma typically appears more lobular and has greater diffusion restriction than OID on DWI  Metastases are usually brighter on T2 imaging  One exception -- scirrhous breast cancer metastasis, which commonly produces a T2-hypointense, fibrotic mass with variable amount of traction on adjacent structures  Benign tumors, such as solitary fibrous tumor, can also show marked T2 hypointensity and overlap with OID in appearance
  • 54.
  • 55. DIFFUSE OID  Seen in 11 % of patients  Patients must be evaluated for systemic disease, including vasculitis and autoimmune conditions such as Churg-Strauss disease or Wegener’s granulomatosis  Common characteristics of orbital involvement in Wegener’s include diffuse infiltration of orbital fat and sinonasal destructive changes  Chest imaging and an immunologic workup are suggested prior to biopsy of diffuse OID  Lymphoma may also mimic diffuse OID and appears more lobular and best distinguished from OID using DWI MRI  Chronic inflammation often contains regions with varying degrees of fibrosis -- heterogeneous appearance on MRI
  • 56.
  • 57. ORBITAL APICITIS  Involvement of the orbital apex  Less common  Associated with the poorest outcome  Inflammatory lesions of the orbital apex are at risk of invading the optic nerve or extending into the cavernous sinus MRI, fat-saturated, T1-weighted image with white arrows showing extension into the cavernous sinus
  • 58.  Tolosa-Hunt syndrome is a rare clinical condition caused by cavernous sinus inflammation presenting with relapsing/remitting acute orbital pain and paralysis of cranial nerves Ⅲ, Ⅳ, Ⅴ1, and Ⅵ  Extension of OID into the cavernous sinus is a common cause of this clinical condition  On T1 MRI, inflammation appears as an intermediate intensity lesion, as inflammatory tissue replaces the normal high-intensity fat at the orbital apex  OID of the orbital apex appears hypointense on T2, with a darker signal indicating higher degrees of fibrosis.
  • 59. D/D  Meningioma, granulomatous disease, and local spread of central nervous system (CNS) pathology  Common features of CNS involvement include abnormal soft tissue extending into the middle cranial fossa, expansion of the ipsilateral cavernous sinus walls, and post-gadolinium enhancement of the meninges or dura
  • 60.
  • 61. INVESTIGATIONS  CBC with ESR  ANA  S.ACE  C-ANCA and p-ANCA  BUN/creatinine  FBS /HBA1C Biopsy may be considered if there are progressive neurologic deficits, lack of steroid responsiveness and persistent imaging abnormalities.
  • 62. Imaging -CT and MRI findings • Orbital CT with contrast : may show thickened posterior sclera ,orbital fat , lacrymal gland involvement or thickening of EOM • Orbital MRI with contrast and fat suppressed : may show EOM enlargement ,orbital fat infiltration ,lacrymal gland enlargement , thickening of posterior tenon / sclera and enhancement along the optic nerve
  • 63. Differential Diagnosis  Thyroid related orbitopathy  Orbital cellulitis +/- Abscess  Non infectious OID : sarcoidosis , IgG 4 reated orbitopathy ,amyoidosis ,eosinophelia ,,GPA ,RA,SLE ,Sjogrens syndrome  Lymph proliferative diseases  Primary orbital malignancy  Metastasis  Vascular malformations : CCF  Cavernous hemangioma
  • 64. Treatment  Observation  NSAIDS  High dose steroid – Acute/Subacute OID. Prednisoone -1 mg /kg/day Tapering should be done over months  Low dose Radiotherapy  Methotrexate ( 15 – 20 mg ),cyclophosphamide -steroid sparing agent  MMF ,Azathioprine ,  Calcineurin nhibitors : cyclosporine, tacrolimus  Refractory cases – Anti TNF – alpha inhibitors  Biologic therapy -I.V infliximab, S.C Adalimumab and Etanercept