Orbital Masses Flashcards

1
Q

What is the most common cause of unilateral or bilateral proptosis in adults?

A

Graves’ Orbitopathy

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2
Q

What is the most common primary benign and malignant orbital tumors in adults?

A

Benign: Cavernous Hemangioma

Malignant: Lymphoma

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3
Q

What is the most common cause of unilateral proptosis in children?

A

Complication 2o sinusitis

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4
Q

What ist he most common benign and malignant orbital tumors in children?

A

Benign: Dermoid (epidermoid/teratoma), capillary hemangioma

Malignant: Rhabdomyosarcoma, #2 glioma

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5
Q

What are the five most common primary orbital tumors overall

A

“Men Have Lived In Orbit”

M: Meningimoa (30%)
H: Hemangioma
L: Lymphoma
I: Inflammatory tumors
O: Optic nerve glioma

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6
Q

List a complete differential of orbital tumors, including primary and secondary orbital tumors

A

EPITHELIAL:
1. Dermoid cyst
2. Simple epithelial (conjunctival) cyst
3. Mucocele
4. Lacrimal (50% benign - pleomorphic adenoma; 50% malignant - ACC, MEC, mixed, adenocarcinoma)
5. SCC
6. BCC (90% of eyelid tumors)
7. Metastasis

MESENCHYMAL:
1. Fibrous dysplasia
2. Rhabdomyosarcoma
3. Osteoma
4. Osteosarcoma

VASCULAR:
1. Hemangioma (cavernous or capillary)
2. Lymphangioma

NEURAL:
1. Meningioma
2. Schwannoma
3. Optic nerve glioma

HEMATOPOIETIC:
1. Lymphoma
2. Leukemia (Chloroma)
3. Histiocytosis

INFLAMMATORY:
1. Pseudotumor
2. Graves (most common in adults)
3. Infection (Viral, bacterial, fungal)
4. Vasculitis (WG, PAN, TA, SLE)

Non-epithelial = fat, fibrous, muscle, bone, cartilage, vessel, nerve, white cells

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7
Q

What are indications for orbital exenteration?

A

INVOLVEMENT OF:
1. Orbital fat
2. Orbital muscle
3. Infraorbital nerve
4. Orbital apex
5. Posterior ethmoid
6. Periorbita/retrobulbar fat
7. Conjunctiva/sclera
8. Painful eye movement

Controversial if vision is normal

Consider the consequences of RT: Diplopia, painful movement or delayed vision loss

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8
Q

What types of tumors can metastasize to the orbit?

A
  1. Breast
  2. Lung
  3. Prostate
  4. GI
  5. Renal cell
  6. Thyroid
  7. Melanoma

Represents 8% of all orbital tumors; 25% will be the presenting manifestation of the original cancer

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9
Q

What is the difference between proptosis and exophthalmos?

A

Proptosis = Pushing of the globe

Exophthalmos = Uniform expansion of the orbital contents

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10
Q

What are 5 non-neoplastic extraorbital causes of proptosis?

A
  1. Mucocele
  2. Trauma or orbital fracture
  3. Cellulitis/abscess
  4. Cavernous sinus thrombosis
  5. Sinusitis complications (most common in children)
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11
Q

What is a neoplastic extraorbital cause of protosis?

A

Lymphoma

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12
Q

What is the average volume of the orbital cavity?

A

30mL

5mL increase in size (16%) will cause 5mm proptosis

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13
Q

Regarding Grave’s Ophthalmopathy, discuss:
1. Epidemiology
2. Pathophysiology

A

EPIDEMIOLOGY
- 3:1 female predominance
- 5th-6th decades
- Incidence 10-45%
- Worse in active smokers
- Most severe forms with CN2 involvement rare
- ~2-5% of Graves’ patients require surgical intervention

PATHOPHYSIOLOGY:
- Due to Thyroid stimulating immunoglobulins (TSI/TSHr antibody)
- T-lymphocyte infiltration into orbital tissues
- Fibroblast response causes Glycosaminoglycan (GAGs) and collagen deposition in the extraocular muscles leading to fibrosis and ophthalmoplegia
- Lid retraction from adrenergic stimulation –> fibrosis of the superior tarsal muscle (Muller’s)
- Initial inflammatory phase, then fibrotic

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14
Q

Outline the Wermer’s Classification of Grave’s ophthalmopathy

A
  • 0: Normal
  • I: Only signs, no symptoms (lid retraction, lid lag, and stare)
  • II: Soft tissue swelling with symptoms and signs (deep conjunctival injection, mild chemosis, edema of caruncle or periorbita)
  • III: Proptosis (≥3mm, use exophthalmometer) with or without symptoms
  • IV: Extraocular muscle involvement (inferior and medial rectus most common, use forced duction test)
  • V: Corneal exposure
  • VI: Sight loss

Forced duction test used to evaluate extraocular muscle entrapment. The examiner uses forceps to grasp the conjunctiva near the attachment of the inferior rectus muscle and attempts to move the globe through a full range of motion.

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15
Q

What is pathognomic for Grave’s orbitopathy on physical exam?

A

Hyperemia over the lateral rectus muscle

https://www.researchgate.net/profile/Adrian-Fung-3/publication/232742013/figure/fig1/AS:931978555703301@1599212411200/A-Clinical-photograph-of-a-patient-with-thyroid-eye-disease-showing-bilateral.png

Vancouver page 101

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16
Q

What are the 2 extraocular muscles most commonly affected in Grave’s ophthalmopathy?

A
  1. Inferior rectus
  2. Medial rectus

Will be seen as an increase in muscle size on CT

17
Q

Describe the medical management of Grave’s Orbitopathy

A
  1. Local Eye Care
    - Eye drops
    - Nocturnal eye taping
    - Sunglasses
  2. Thyroid therapy
    - Antithyroid drugs (e.g. PTU, Methimazole)
    - Radioiodine ablation
    - Thyroidectomy
  3. Steroid therapy
    - For acute vision loss, Prednisone 80-120mg daily x 2 weeks with slow taper
  4. Immunosuppressives
    - Cyclosporine
    - Cyclophosphamide experimental for autoimmune aspects
  5. Radiotherapy
    - Indicated for late sequelae of stable thyroid orbitopathy
    - 20 Gy in 10 fractions (2 weeks) - good-excellent response in 35-92%, not for acute/subacute phases, for those who can’t tolerate/refuse/fail surgery
  6. Beta-blockers
    - Propranolol can be used as adjunct for severe symptoms
18
Q

Indications for orbital decompression in Graves Orbitopathy

A
  1. Altered vision/blindness - decreased acuity, field defects, abnormal visual evoked potentials, disk edema; typically, after failed course of steroids
  2. Corneal exposure keratitis not responding to medical therapy
  3. Cosmetic decompression only if eye findings stable for at least 6 months
19
Q

What are the surgical options for Grave’s orbitopathy?

A
  1. Naffziger: Superior orbital plate decompression into anterior cranial fossa
  2. Kronlein: Lateral orbital plate through coronal, direct rim incision or lateral canthotomy
  3. Hirsch: Inferior orbital plate through subciliary and/or Caldwell-luc incision
  4. Sewall: Medial orbital decompression through coronal incision or external ethmoidectomy approach
  5. Walsh-Ogura: Transantral decompression of medial/inferior orbit, most widely used, as it is extracranial & decompresses two orbital walls into the largest empty space, allows gravity to aid in the expansion (traditionally gone through the caldwell-luc approach)
  6. Orbital fat removal: Through upper lid crease and subciliary approaches, ~6mm maximum reduction in proptosis possible
  7. Endoscopic orbital decompression: Transnasal or external - ligate AEA and PEA - longitudinal periorbital incision
20
Q

What is a Chloroma?

A

aka. Granulocytic sarcoma

  • Immature myeloid cell collection seen in AML and CML
  • Green color secondary to myeloperoxidase
  • Symptoms: Painless proptosis & violaceous lid, swelling over weeks
  • Treatment: Systemic chemotherapy ± EBRT (will develop into leukemia without treatment)
  • Prognosis - poor, death usually within 18 months
21
Q

Regarding optic nerve glioma, discuss:
1. Epidemiology
2. Cell origin
3. Radiographic findings
4. Treatment

A

EPIDEMIOLOGY:
- 2nd most common pediatric orbital tumor

CELL ORIGIN:
- Fibrillary astrocyte, associated with neurofibromatosis in 18-50%

RADIOGRAPHIC FINDINGS:
- CT fusiform (tapered at both ends like a spindle), lobular, isodence homogeneous enlargement of optic nerve
- MRI: T1 hypo, T2 hyper

TREATMENT:
- Observation vs. resection depending on whether indolent or progressive growth

22
Q

Regarding Orbital pseudotumor, discuss:
1. What is it?
2. Signs and symptoms
3. Radiographic findings
4. Treatment

A

ORBITAL PSEUDOTUMOR:
- Inflammation of unknown etiology, diffuse or localized (muscle, lacrimal gland, sclera, optic nerve)
- Likely an IgG4-related disease

SIGNS/SYMPTOMS:
1. Signs: Eyelid edema, chemosis, diplopia, vision loss (20%)
2. Symptoms: Pain worsened with movement, proptosis

RADIOGRAPHIC:
- CT enlargement of involved structures
- EOM tendons involved unlike in Graves’ ophthalmopathy
- MRI T1 iso to muscle with gad enhancement, T2 hyper to fat

TREATMENT:
1. Corticosteroids
2. Rarely Cyclophosphamide, Cyclosporine, or XRT
3. Biopsy treatment failures!