Ocular Disease: Lecture 2: Orbital Vascular Anomaly Flashcards
- Carotid Cavernous Fistula: 2 types?
- Direct and Indirect
Carotid Cavernous Fistula (1)
- Define
- Arterialization of Venous BF
a. What happens with Venous pressure
b. Arterial BF?
c. What happens to Arterial Pressure? Why?
- A/V fistula b/w the ICA and the Cavernous Sinus
- a. Increases. You get Retrograde flow of arterial blood into Orbit via Ophthalmic Veins
b. Decreased Arterial BF to Cranial Nerves
c. Decreases. It’s kind of like a leaky pipe…decreased arterial BF due to decreased arterial pressure
Carotid Cavernous Fistula
- Etiology (2)?
- Hemodynamics (2)?
- Anatomy (2)?
- Spontaneous or Traumatic
- High (ICA) or Low
- Direct or Indirect (High Volume, High BF)
Direct Carotid Cavernous Fistula
- % of cases?
- High Flow shunts: Why?
- Caused by what 2 things?
- 50% of all cases
- Blood flows DIRECTLY from intrcavernous portion of ICA to cavernous sinus via WALL DEFECT
- Trauma (75%) or Spontaneous (25%)-generally lower flow and Less symptomatic.
* Generally, spontaneous are Burst aneurysms (usually middle Age Women who are Hypertensive)
Direct Carotid Cavernous Fistula (2)
- Clinical Triad?
- Ipsilateral to insult or bilateral/contralateral?
- a. Pulsatile Proptosis (associated w/Bruit and ALLEVIATED w/Ipsilateral Carotid Compression)
b. Conjunctival Chemosis (Swollen, can’t close Eyelids)
c. “Whooshing” noise (supposedly happens w/Cavernous sinus fistula) - Usually Ipsilateral to Insult, but can also be Bilateral or Contralateral.
Direct Carotid Cavernous Fistula (3)
Other Signs
- What happens to Epibulbar?
- Type of Chemosis?
- Ptosis?
- IOP?
- What can happen to the Anterior Segment?
- What is seen 60-70% of the time?
- Severe Epibulbar Injection (blood has no where to go. Backs up and we see a LOT of vascular injection)
- Hemorrhagic Chemosis
- Possible Ptosis
- Elevated IOP
- can have Anterior Segment Ischemia
- Ophthalmoplegia. (6th nerve is most common and you can get Engorgement of EOMs)
Direct Carotid Cavernous Fistula (4)
- Vision: Immediate Loss due to what?
- Vision: Delayed loss can lead to what 5 things?
- What palsy is seen?
- due to ON damage at time of injury
2. Anterior segment Ischemia, CRV occlusion, Exposure keratopathy, Ischemic Optic Neuropathy, and 2ndary Glaucoma
Direct Carotid Cavernous Fistula (5)
Testing
- CT and MRI: to see what?
- What is the definitive test?
- Engorgement of Superior Ophthalmic Vein
2. CT and MRI Angiography
Direct Carotid Cavernous Fistula (6)
- When is treatment necessary?
- What can they do to treat it?
- only if spontaneous closure doesn’t happen
2. Endovascular Embolization: Coils or Balloons.
Indirect Carotid Cavernous Fistula (Dural Shunt) (1)
- Communication with what exactly?
- Blood flow level?
- Causes? (2/3)
- w/Meningeal Branch of the ICA or ECA, or both
- Low flow
- Congenital Malformations
and
Spontaneous Rupture (HTN Patients (constipation) or caused by Minor trauma or Valsalva)
Indirect Carotid Cavernous Fistula (Dural Shunt) (2)
- How does it present? (2)
- What is exaggerated?
- IOP level?
- Gradual onset; Epibulbar injection WITH or W/O Chemosis (can be unilateral or bilateral)
- Ocular pulsation (noted on tonometry)
- Elevated IOP
Indirect Carotid Cavernous Fistula (Dural Shunt) (3)
- Epibulbar Vessels: What happens to them?
- Proptosis possible?
- Ophthalmoplegia?
- Fundus?
- Corsckrew Epibulbar Vessels (Late sign)
- Mild proptosis possible
- 6th nerve and EOM Congestion
- can be normal or may demonstrate venous dilation
Indirect Carotid Cavernous Fistula (Dural Shunt) (4)
- Treatment?
- Similar to DIRECT, but us must use a TRANS VENOUS METHOD
Thyrotoxicosis (Hyperthyroidism) (1)
- What is it?
- What does it lead to?
- 2 things that cause it?
- Female:male ratio?
- Can be associated with what disorders?
- Over production of thyroid hormones
- Elevation of BMR
- a. Graves (85% of hyperthyroidism; AI)
b. Toxic nodular goiter and Thyroiditis - 10:1
- with other AI disorders
Thyrotoxicosis (Hyperthyroidism) (2): Presentation
- What age?
- Signs overall? (8)
- 3rd to 4th decade
- Heat intolerance, Irritability, Increased bowel movements, Nervousness, Palpitations, Sweating, Weakness and fatigue, and Weight loss
Thyrotoxicosis (Hyperthyroidism)
(3)
- External Signs? (8)
- Alopecia
- Finger clubbing and plummers nail
- Hand Tremor
- Pretibial Myxedema
- Reddening of the palms
- Thyroid Enlargement
- Vitiligo
- Warm, sweaty skin
Thyrotoxicosis (Hyperthyroidism) (4)
- Cardiovascular signs? )(4)
- Atrial Fibrillation
- High output heart failure
- Premature ventricular beat
- Sinus tachycardia
Thyroid Eye Disease (Ophthalmopathy) (1)
- When can it occur?
- Is it dependent upon anything systemic?
- Major risk factor?
- More likely in whom?
- Anytime
- No. Independent of Systemic sx/sn
- Smoking (increased cigarettes/day = increased risk for TED)
- 5x’s more likely in women
Thyroid Eye Disease (Ophthalmopathy) (2)
- Pathogenesis
a. Cause?
b. What does it do to EOMs?
c. Leads to what?
d. What EOM is most common?
- a. AI reaction (rx)
b. Inflammation of EOMs (can enlarge up to 8x’s normal size)
c. Fibrosis
d. IR, then MR, SR and finally LR
Thyroid Eye Disease (Ophthalmopathy) (3)
- Clinical manifestations? (5)
- a. Lid retraction
b. Optic Neuropathy
c. Proptosis
d. Restrictive Myopathy
e. Soft tissue involvement
Thyroid Eye Disease (Ophthalmopathy) (4)
- Stages of TED and what happens in each?
- Congestive (Inflammatory)
a. Red painful eyes
b. Remits after 3 years
c. about 10% develop long term complications - Fibrotic Stage
a. White and Quiet
b. Painless Motility Defect
Thyroid Eye Disease (Ophthalmopathy) (5): Soft Tissue Involvement
- 3 Signs?
- 5 Symptoms?
- a. Epibulbar Hyperemia
b. Periorbital Swelling (Chemosis, Prolapse of fat into eyelid) - a. Discomfort behind eyes
b. Dryness
c. Grittiness
d. Lacrimation
e. Photophobia
**Sausage like rolls (Prolapse of fat into eyelid)