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Case Analysis I- Lecture 9 Liana Al-Labadi, O.D.

Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

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Page 1: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Case Analysis I- Lecture 9

Liana Al-Labadi, O.D.

Page 2: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

If you hear hoof beats, think horses—not

zebras

Page 3: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

CC: Dr. I see a black curtain over my

eyes

Page 4: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black” Frequency: Constantly (all the time, everyday) @ D&N Onset: Suddenly10 days ago, but has noticed it more

over the past 2 days Location: Both eyes Duration: Lasts for a short time but I feel it’s there all

the time Associated Factors:

Blurry vision A lot of headaches

Relief: Headaches get better with parcetamol but I still see a

black curtain Severity:

The blacking out is pretty bad, I just can’t stand it anymore. The headaches are there all the time.

Page 5: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

DIFFERENTIAL DIAGNOSIS????

Page 6: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black” Migraine DES / Keratitis/ Blepharitis/ Iritis /AACG Vitreous detachment /Retinal break Angiospasm/ vasospasm Optic disc drusen/ Orbital tumor Papilledema ON / MS/ SLE Embolic/ Carotid emboli / Cardiac emboli IV drug use Hypoperfusion Coagulation disorders /Inflammatory arteritis Carotid stenosis /Ophthalmic artery stenosis Cardiac failure or arrhythmia Increased blood viscosity Intraocular hemorrhage Intracranial tumor Psychogenic

Page 7: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

POH: (+) Near sightedness Negative for asthenopia, surgery, pain, & flashes Negative for AMD, DR, Cats & Glc (+) DIPL-?????? (+) Trauma- 14 years ago?????

LEE: 6 months ago (unknown doctor)- Status normal FOH: Negative for AMD, DR, Glc, Cat LPE: Does not remember PMH:

(+) stress (+) ENT (+) Respiratory Negative for HTN/DM/Cancer/Neuro

FMH: (+) HTN- Father; (+) DM- Parents; Migraines- Parents MED: None Allg: NKDA; No seasonal allergies SH: Reading Occupation: Student No alcohol consumption ; (+) smoking- Argeeleh

“Dr. I See All Black”

Page 8: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Entrance Testing: DVA (c):

OD: 20/50 PH: ??????????? OS: 20/30 PH: ???????????

Motility: S&F OD, OS Pupils: 4mm/4mm RRL OD, OS; No APD Confrontations:

OD: Slight inferior constriction OS: Full

“Dr. I See All Black”

Page 9: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Additional Tests: Lensometry:

OD: -3.75 -0.50x 153 OS: -3.75 -0.50x 153

Manifest Refraction: OD: -4.00 -0.50x 165 VA: “All black” OS: -3.75 -0.50x 153 VA: “All black”

“Dr. I See All Black”

Page 10: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

SLE: L/L: trace MGD OD, OS Conj: No injection OD, OS K: Clear OD, OS Iris: Flat & brown OD, OS AC: No cell & no flare/ D&Q OD, OS Lens: Clear OD, OS

IOP (TA): ??????????

“Dr. I See All Black”

Page 11: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black”

Page 12: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black” DFE:

CDR: 0.15 round OD, OS NRR: 360˚ optic nerve swelling/elevation OD, OS

Blurry disc margins OD, OS Superior flame-shaped heme OD Inferior flame-shaped heme OS

Macula: Flat OD, OS Posterior Pole: Flat OD, OS Vessels:

Dilated & tortuous OD, OS Periphery: ????

Page 13: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black” Differential Diagnosis:

Papilledema Retinal Vein Occlusion Optic Neuritis/Papillitis Ischemic Optic Neuropathy Compressive Optic Neuropathy Infiltrative Optic Neuropathy Systemic etiology:

Sarcoid Leukemia

Page 14: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black” Assessment:

Bilateral optic never disc edema Unknown etiology Sx of TVO + Headaches + DIPL

Plan:Pt education on condition Refer for CT scanRefer patient for neurological work-upPt education on importance of follow-up with

neurology appointment

Page 15: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black” F/U Visit:

Patient was told it was “benign” Began oral medications

Page 16: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black” Assessment:

Bilateral Papilledema

Plan:RTC in 2 months for DFE + Visual Field

Page 17: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema-Definition Optic disc swelling produced by increased

intracranial pressure

Page 18: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema-Symptoms Symptoms:

Episodes of transient, often bilateral visual loss Lasting seconds

Symptoms precipitated after rising from a lying or sitting position (altering intracranial pressure)

Headache Double vision Nausea Vomiting Tinnitis Decrease in visual acuity (rare)

Mild decrease in VA can occur in an acute setting if there is macular disturbance

Visual field defects & severe loss of central vision Occur only with chronic papilledema

Page 19: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema-Signs Critical Signs:

Bilaterally swollen, hyperemic discs Early papilledema- disc swelling may be asymmetric

NFL edema causing blurring of the disc margin and often obscuring the blood vessels

Other Signs: Papillary pr peripapillary retinal hemorrhages Loss of venous pulsation

20% of the normal population do not have venous pulsation

Dilated, tortuous retinal veins Normal pupillary response Normal color vision Enlarged blind spot

Page 20: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema-Signs Signs of chronic papilledema:

Any hemorrhages or cotton-wool spots resolve Disc hyperemia disappears The disc becomes gray in color Narrowing of the peripapillary retinal vessels Optociliary shunt vessels may develop on the disc Loss of color vision, VA, VF defects (especially inferionasally)

may also occur

Page 21: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

“Dr. I See All Black”

Page 22: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema Differential Diagnosis

Other Differential Diagnosis: Pseudopapilledema

Not true disc swelling Vessels overlying the disc are not obscured The disc is not hyperemic The surrounding NFL is normal Spontaneous venous pulsation is often present

Secondary to optic disc drusen or congenitally anomalous disc Hypertensive optic neuropathy

Optic nerve disc swelling caused by extremely high blood pressure

Narrowed arterioles A/V crossing changes Heme with or with out CWS in the peripheral retina and

posterior pole

Page 23: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema Differential Diagnosis Other Differential Diagnosis:

Orbital optic nerve tumors: Unilateral disc swelling May have proptosis

Amiodarone toxicity Patient present with acute visual loss and disc edema

Diabetic papillopathy: Benign disc edema in one or both eyes of a diabetic

patient Telagectasia of BVs and NV of the disc may occur

Thyroid-related optic neuropathy:

Page 24: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema Etiology Primary & metastatic intracranial tumora Hydrocephalus Pseudotumor cerebri (PTC) Subdural & epidural hematomas Subarachnoid hemorrhage

These patients have severe headaches Arteriovenous malformation Brain abscess- often produces high fever Meningitis

Fever, stiff neck, headache Encephalitis Cerebral venous sinus thrombosis

Page 25: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema Work-Up History & physical examination

Including blood pressure measurement Ocular examination

Pupils, color vision, DFE, VF Emergency MRI with MRV (magnetic

resonance venography) of the head CT scan may be done if MRI is not available

emergently Lumbar puncture with CSF analysis and

opening pressure measurement Done if MRI/MRV or CT scan results are normal

Page 26: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Papilledema Treament Treatment

Directed at the underlying cause of the increased intracranial pressure

Page 27: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Pseudotumor Cerebri (PTC) AKA Idiopathic Intracranial Hypertension (IIH) A syndrome in which patients present with

symptoms and signs of elevated intracranial pressure The nature of which may be idiopathic or due to

various causative factors Diagnosis of exclusion

Need to eliminate all other possible etiologies

Page 28: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Pseudotumor Cerebri (PTC) Symptoms:

Headaches Between 90% and 98% of patients with IIH present with

headache TVO

Transient episodes of visual loss- typically lasting seconds Percipitated by changes in posture

Double vision Tinnitis Nausea Vomitting Occurs predominantly in obese women of childbearing

age (20 to 44 years) “Fat 40 disease” Some studies suggest that excess weight in the abdominal

area causes a chain reaction from increased intra-abdominal pressure, eventually leading to increased intra-cranial venous pressure

Page 29: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Pseudotumor Cerebri (PTC) Critical Signs:

Papilledema due to increases intracranial pressure Bilateral papilledema is a hallmark sign of the disease

Negative MRI/MRV of the brain MRV added to evaluate the venous system of the brain and to

rule out a sinus thrombosis that is usually missed with an MRI. Without this information, the patient with a sinus thrombosis

could be misdiagnosed with the more benign PTC Increased opening pressure on lumbar puncture with

normal CSF composition Opening pressure exceeds 250mm of water

Other Signs: Unilateral or bilateral 6th nerve palsy with no other

neurological signs

Page 30: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Pseudotumor Cerebri (PTC) Differential Diagnosis:

Same as Papilledema- refer to previous slides

Page 31: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Pseudotumor Cerebri (PTC) Associated Factors:

Obesity “Fat 40” Significant weight gain Pregnancy Medications:

Oral contraceptives Tetracyclines Nalidixic acid Cyclosporine Vitmain A (>100,000 U/day) Systemic steroid withdrawl

http://www.revoptom.com/content/d/cornea/c/15325/

Page 32: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Pseudotumor Cerebri (PTC) Work-Up:

History: Specifically inquire about weight gain & medications

Ocular Exam: Pupils, EOMs, color vision & optic nerve evaluation Visual field test- very important for following up patients

Systemic Exam: Measure blood pressure & temperature Thorough blood work with CBC to R/O infectious

etiologies MRI/MRV of orbit and brain

Must be done immediately Need to R/O a space-occupying lesion

If normal refer for neuro-ophthalmic evaluation, including a lumbar puncture, to rule out other causes of papilledema & to determine the CSF opening pressure

Page 33: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Pseudotumor Cerebri (PTC) Treatment:

PTC may be a self-limited process. Treatment is indicated in the following situations:

Severe, intractable headaches Evidence of progressive decrease in visual acuity or visual

field loss Some ophthalmologists suggest treating all patients with

papilledema Method of treatment:

Wight loss- if overweight or recent increase in weight – 1st line tx

Acetazolomide (Diamox) Use with caution in sulfa-allergic patients Can decrease CSF production by 50%

Discontinuation of any causative medication If method of treatment unsuccessful

Consider systemic steroids Optic nerve sheathing surgery if reduced VA Neurosurgical shunt if headaches are a prominent symptom

Page 34: Case Analysis I- Lecture 9 Liana Al-Labadi, O.D

Pseudotumor Cerebri (PTC)

Prognosis: Typically good if the underlying condition is

addressed promptly Follow-Up:

If acute: Monitor every 3 months in the absence of visual field loss

If chronic: Initially follow-up every 3-4 weeks to monitor visual

acuity and visual field loss then every 3 months

Patient education: Educate patients that papilledema can lead to optic

atrophy & irreversible vision damage if left untreated